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Objective To analyze the differences in the expressions of the total and phosphorylated proteins in human colon cancer HCT116 cells after the knockout (KO) of retinoic acid-induced protein 16 (RAI16) and explore the possible mechanism and related signaling pathways affecting its protein function in HCT116 cells. Methods HCT116 KO and WT cell proteins were collected and extracted, and the protein extraction efficiency was detected via a sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) experiment. After protein digestion, the peptides were labeled with TMT and analyzed via mass spectrometry. We used bioinformatics methods to analyze the identified differential proteins and differentially phosphorylated proteins by using GO, KEGG, and STRING databases. Results The results of SDS-PAGE showed no evident protein degradation. In addition, some key bands were significantly different between the experimental and control groups. A total of 147 up-regulated and 230 down-regulated differential proteins were screened in accordance with the conditions of Foldchange≥1.5 or Foldchange≤1/1.5 and P<0.05. Meanwhile, 106 up-regulated and 217 down-regulated phosphorylation sites were screened. GO enrichment analysis revealed that the differential proteins were mainly enriched in the composition of nucleoplasm, nucleus and cytoplasm, RNA binding, cadherin and chromatin, DNA repair, RNA splicing, and positive regulation of DNA as template transcription. The results of KEGG enrichment indicated that the differential proteins were mainly enriched in nucleocytoplasmic transport, spliceosomes, cell cycle, cell-cell tight junctions, viral carcinogenesis, microRNAs in cancer, etc. The protein interaction network mainly focused on DDX17, NCL, EEF2, CDK1, SSRP1, and SMARCC1. The statistical findings unveiled the up-regulated changes in the two omics of SKP1, ORC1, and BAD and the down-regulated changes in RBL1, RB1, CDK1, CDC6, MCM4, TFDP1, CHD4, and SNW1. Moreover, the phosphorylation differences were more significant than the protein differences. Conclusion RAI16 plays the possible crucial role in multiple biological functions and signaling pathways through key proteins, such as SKP1, ORC1, RB1, and CDK1, which affect the cell cycle and thereby the occurrence and development of cancer [ABSTRACT FROM AUTHOR]

Objective To explore the correlation of RELL1 expression with clinical pathological features and prognosis of patients with colon cancer. Methods Immunohistochemical experiments of the RELL1 protein were performed on tissue chips from 80 colon cancer tissues and 80 adjacent tissues. The relationship between different expression levels of RELL1 protein and clinical pathological parameters was compared. Univariate and multivariate Cox risk proportional regression analyses were conducted on factors affecting the survival of patients with colon cancer. Kaplan-Meier survival curve analysis was conducted on the survival rates of patients with colon cancer and different levels of RELL1 expression. Log rank test was performed to evaluate differences in survival rates. Results The expression of RELL1 in colon cancer tissues was lower than that in adjacent tissues (P<0.05). The expression of RELL1 in cancer tissues is correlated with TNM stage and N stage (P<0.05). The 3-year overall survival (OS) rate of colon cancer patients with high RELL1 expression was higher than that of patients with low RELL1 expression (P<0.05). Multivariate Cox regression analysis showed that low RELL1 expression, advanced age, and high TNM stage were risk factors for poor prognosis in patients with colon cancer (P<0.05). Conclusion The expression of RELL1 is downregulated in colon cancer tissue, and the low RELL1 expression, advanced age, and high TNM stage can lead to adverse outcomes in patients [ABSTRACT FROM AUTHOR]

Background and purpose: Currently, for patients with mid-to-low locally advanced rectal cancer and potentially resectable T4bM0 colon cancer, guidelines recommend neoadjuvant therapy strategies to enhance the response rate and increase the likelihood of conversion surgery. Among these patients, ypⅢ stage colorectal cancer (CRC) is assessed using the Union for International Cancer Control (UICC)/American Joint Committee on Cancer (AJCC) TNM staging system for postoperative pathological features. However, neoadjuvant therapy can lead to lymph node regression in the surgical area, resulting in an insufficient number of detected lymph nodes (less than 12), preventing classification according to conventional TNM staging. Thus, TNM staging often fails to predict the prognosis of ypⅢ patients who have undergone neoadjuvant therapy. This study aimed to evaluate the prognostic value of the positive lymph node ratio (LNR) in ypⅢ stage CRC patients treated with neoadjuvant therapy. Methods: Retrospective data was collected from ypⅢ stage CRC patients who received neoadjuvant therapy and underwent radical surgery at Fudan University Shanghai Cancer Center between 2008 and 2018. Collect clinical pathological characteristics such as age, gender, primary tumor location, tumor differentiation grade, pathological staging, and whether the patient has relapsed or died during follow-up at the time of surgery. Inclusion criteria: CRC patients who have received neoadjuvant therapy and surgery and have been confirmed to be stage Ⅲ by postoperative pathological examination. Exclusion criteria: ① Preoperative imaging examination or intraoperative exploration reveals distant organ metastasis; ② History of malignant tumors in the past; ③ Multiple primary CRC. This study was approved by the medical ethics committee of Fudan University Shanghai Cancer Center (ethics number: 050432- 4-2108*). The R software survminer package (surv_cutpoint algorithm) was used to calculate the optimal cutoff value for LNR relative to disease-free survival (DFS), and patients were divided into low and high LNR groups accordingly. Clinical pathological characteristics and DFS were compared between the two groups. COX proportional hazards regression models were employed to identify adverse pathological features, and survival plots along with prediction models for DFS were generated using the survival and rms packages. Results: A total of 489 patients were included, comprising 289 males and 200 females, with a median age of 56 years (23-80 years) and a median follow-up time of 1 062 d. During the follow-up period, 164 patients (33.5%) died. In the entire cohort, 204 (41.7%) patients had fewer than 12 lymph nodes detected. The optimal cutoff value for LNR was 0.29, classifying 317 patients into the low LNR group (LNR≤0.29) and 172 patients into the high LNR group (LNR＞0.29). The high LNR group exhibited shorter DFS compared to the low LNR group [hazard ratio (HR)=2.103, 95% CI: 1.582-2.796, P＜0.000 1]. Multivariate COX regression indicated that LNR was an independent prognostic factor for DFS (HR=1.825, 95% CI: 1.391-2.394, P＜0.001). The inclusion of LNR in a multicategory DFS nomogram prediction model effectively assessed DFS in stage Ⅲ CRC patients who had undergone neoadjuvant therapy. Conclusion: LNR is an independent prognostic factor for ypⅢ stage CRC patients, showing good predictive power for DFS when combined with other adverse pathological features. Therefore, incorporating LNR as a supplement to TNM staging can improve the accuracy of CRC prognosis assessment. [ABSTRACT FROM AUTHOR]

AIM: To investigate the effects of γ-synuclein on autophagy and apoptosis of colon cancer cells induced by endoplasmic reticulum stress, as well as the protective effect on the cells. METHODS: Gene expression profile chip analysis was performed to compare the cDNA expression profiles between human colon cancer HCT116 cells with γ-synuclein knockdown and HCT116 cells with control siRNA, and to identify potential molecules related to autophagy and apoptosis. In colon cancer cell lines, the functional effects of γ-synuclein on autophagy and apoptosis induced by thapsigargin (TG), an endoplasmic reticulum stress-inducing agent, were systematically explored by conducting immunofluorescence staining, Western blot, CCK-8 assay, flow cytometry, and transmission electron microscopy. Western blot was used to detect the expression of γ-synuclein protein, autophagy-related proteins [microtubule-associated protein 1 light chain 3 (LC3), beclin-1, autophagy-related protein 5 (ATG5) and ATG7], and apoptosis-related proteins [poly (ADP-ribose) polymerase (PARP), pro-caspase-3, and pro-caspase-9]. To further analyze the mechanism of γ-synuclein in regulating autophagy and apoptosis, extracellular signal-regulated kinase (ERIK) inhibitor PD98059, ERII inhibitor SP600125 and c-Jun N-terminal kinase (JNII) activator anisomycin were applied separately to test HCT116 cells transfected with 7-synuclein siRNA. Subsequently, autophagy proteins, apoptosis proteins, and ERK and JNII pathway-related proteins were detected by Western blot. RESULTS: The TG-induced autophagy of colon cancer cells mainly occurred at the early stage (0~24 h), and apoptosis mainly occurred at the late stage (36~48 h). Endoplasmic reticulum stress up-regulated the expression of γ-synuclein in colon cancer cells, which was associated with enhanced autophagy. γ-Synuclein promoted autophagy by activating ERK and JNII pathways at the early stage (0~24 h), and inhibited apoptosis by blocking JNII pathways at the late stage (24~48 h) to protect HCT116 cells. In our model, γ-synuclein was observed to play a critical role in the transition from endoplasmic reticulum stress-induced autophagy to apoptosis. CONCLUSION: In the context of endoplasmic reticulum stress, 7-synuclein promotes autophagy and inhibits apoptosis by regulating ERK and JNII signaling pathways, thus protecting colon cancer cells. This provides a potential idea for anti-tumor therapy. [ABSTRACT FROM AUTHOR]

ObjectiveTo analyze the differences in the expressions of the total and phosphorylated proteins in human colon cancer HCT116 cells after the knockout (KO) of retinoic acid-induced protein 16 (RAI16) and explore the possible mechanism and related signaling pathways affecting its protein function in HCT116 cells. MethodsHCT116 KO and WT cell proteins were collected and extracted, and the protein extraction efficiency was detected via a sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) experiment. After protein digestion, the peptides were labeled with TMT and analyzed via mass spectrometry. We used bioinformatics methods to analyze the identified differential proteins and differentially phosphorylated proteins by using GO, KEGG, and STRING databases. ResultsThe results of SDS-PAGE showed no evident protein degradation. In addition, some key bands were significantly different between the experimental and control groups. A total of 147 up-regulated and 230 down-regulated differential proteins were screened in accordance with the conditions of Foldchange≥1.5 or Foldchange≤1/1.5 and P

ObjectiveTo explore the correlation of RELL1 expression with clinical pathological features and prognosis of patients with colon cancer. MethodsImmunohistochemical experiments of the RELL1 protein were performed on tissue chips from 80 colon cancer tissues and 80 adjacent tissues. The relationship between different expression levels of RELL1 protein and clinical pathological parameters was compared. Univariate and multivariate Cox risk proportional regression analyses were conducted on factors affecting the survival of patients with colon cancer. Kaplan-Meier survival curve analysis was conducted on the survival rates of patients with colon cancer and different levels of RELL1 expression. Log rank test was performed to evaluate differences in survival rates. ResultsThe expression of RELL1 in colon cancer tissues was lower than that in adjacent tissues (P

Objective To investigate the effect of docosahexaenoic acid (DHA) on human colon cancer cell line HT-29 and underlying mechanism. Methods Human colon cancer cell line HT-29 was incubated with DMSO (control), DHA (25, 50, 100 μmol/L) and 100 μmol/L DHA and/or 30 μmol/L 740Y-P. Proliferation was examined by MTT; apoptosis was detected by annexin V-FITC/PI. Western blot was used for detection of protein expression of Bcl-2, Bax apoptosis-related protein and PI3K/Akt/mTOR pathway, and RT-qPCR was used for checking mRNA expression of NLRP3/Caspase-1/IL-1β pathway. Results Compared with the control group, DHA 25, 50,and 100 μmol/L treatment of HT-29 cells resulted in decreased cell survival (P＜0.05), increased apoptosis(P＜0.05), decreased Bcl-2/Bax ratio(P＜0.05) and decreased phosphorylation of PI3K, Akt and mTOR in HT-29 cells(P＜0.05 or P＜0.01). Expressions of NLRP3, Caspase-1 and IL-1β mRNA were decreased (P＜0.05). In addition, cell viability, protein phosphorylation (p-PI3K, p-Akt, p-mTOR)and relative mRNA expression of NLRP3, Caspase 1, and IL-1β were lower in HT-29 cells which were co-incubated with DHA 100 μmol/L and 740Y-P 30 μmol/L than those in the control group (P＜0.05 or P＜0.01) and 740Y-P 30 μmol/L group (P＜0.05), while higher than that of DHA 100 μmol/L group(P＜0.05 or P＜0.01). Conclusions DHA inhibits the proliferation of human colon cancer cell line HT-29, its mechanism is potentially related to the inhibition of PI3K/Akt/mTOR and NLRP3/Caspase-1/IL-1β signaling pathways.

Objective To explore the expression of serine proteinase inhibitor family E member 1 (SERPINE1) in colon cancer and its effect on the malignant biological behaviors of colon cancer cells. Methods starBase and TISIDB databases were used to analyze the expression of SERPINE1 in 471 patients with colon cancer and 41 paracancerous tissues, and the relationships of its differential expression with clinical stage and prognostic survival were analyzed. The cancer specimens and paracancerous tissues from 5 patients with colon cancer were collected in No. 940 Hospital of Joint Logistic Support Force, and RT-qPCR and Western blotting were employed to detect the expression of SERPINE1 at mRNA and protein levels. After lentiviral vectors of SERPINE1 overexpression and interference were constructed and transfected into colon cancer RKO and LoVo cells. The experimental cells were assessed by RT-qPCR and Western blotting to verify the efficiency of overexpression and interference. Then cell proliferation, migration, invasion and apoptosis were evaluated by CCK-8 assay, clone formation test, Transwell test and Hoechst apoptotic nuclear staining, respectviely. Finally, Western blotting was applied to determine the effect of SERPINE1 on phosphatidyl-inositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. Results Database analysis showed that SERPINE1 was highly expressed, positively correlated with the clinical stage and negatively correlated with the overall survival in colon cancer patients (P < 0.05). Transfection of overexpression lentiviral vector resulted in enhanced cell proliferation, invasion and migration abilities while weakened apoptosis in RKO and LoVo cells. On the contrary, SERPINE1 interference reduced the abilities of cell proliferation, invasion and migration but improved cell apoptosis (P < 0.05). Western blotting showed that overexpression of SERPINE1 had no effect on the expression of PI3K and AKT, but increased the expression of p-PI3K and p-AKT, and SERPINE1 interference also had no change in PI3K and AKT expression and reduced the levels of their phosphorylation levels. Statistical differences were observed in relative quantitative analysis on the ratios of p-PI3K/PI3K and p-AKT/AKT (P < 0.05). Conclusion SERPINE1 is highly expressed, and correlated with clinical stage and prognosis of patients with colon cancer. Its overexpression promotes the proliferation, migration, invasion and inhibits apoptosis of colon cancer RKO and LoVo cells through PI3K/AKT signaling pathway.

Objective To establish a nomogram model to predict the survival of elderly patients with colon cancer after radical resection, and to verify the predictive value of this model. Methods A total of 118 elderly patients with colon cancer who underwent radical surgery at the Xinjiang Medical University Affiliated Traditional Chinese Medicine Hospital from January 2015 to December 2017 were selected as the research subjects. The prognostic indicators of elderly patients with colorectal cancer after radical surgery were analyzed by univariate Cox regression analysis. The meaningful indicators with P0.05). Conclusion The nomogram model combined with differentiation degree, TNM/T staging, lymph node metastasis and VEGF can accurately predict postoperative disease-free survival and overall survival of elderly patients with colon cancer.

Objective To identify small molecule inhibitors of APC-mutant colon cancer and provide lead compounds for targeted therapy of colon cancer. MethodsAPC-mutant colon cancer cell lines that stably express 7*Tcf-GFP/SV40-Cherry (7TGC) dual fluorescence reporter system was constructed for small-molecule inhibitor screening. Cell viability, colony formation, EdU incorporation, and xenograft tumor assay were used to evaluate the inhibitory effect of these inhibitors on APC-mutant colon cancer in vitro and in vivo. Western blot and co-immunoprecipitation assays were used to explore the molecular mechanism. ResultsFour small molecules that inhibited Wnt activity in APC-mutant colon cancer cells were discovered. Shikonin exhibited significant inhibition of cell viability and proliferation while inducing apoptosis of APC-mutant colon cancer cells. Xenograft tumor assay demonstrated that shikonin significantly reduced tumor growth in vivo. Furthermore, Western blot and co-immunoprecipitation assays revealed that shikonin markedly decreased β-catenin levels. ConclusionShikonin effectively inhibits Wnt activity and suppresses tumor growth in APC-mutant colon cancer.

Objective: To verify whether phosphoglycerate mutase 1 (PGAM1) allosteric inhibitor could enhance the sensitivity of colon cancer cells to oxaliplatin (OXA). Methods: OXA sensitivity and PGAM1 expression levels of four consensus molecular subgroups (CMS) of colon cancer cells were analyzed according to genomics of drug sensitivity in cancer (GDSC）and cancer cell line encyclopedia (CCLE) databases. CCK8 assay and Annexin V/PI staining were used to investigate the effect of PGAM1 allosteric inhibitor HKB99 on the proliferation and apoptosis of human colon cancer cell lines. CCK8 assay were performed to investigate the effect of HKB99 combined with OXA on the proliferation of colon cancer DLD-1 cells and cooperativity index was analyzed according to the result. Results: Firstly, GDSC and CCLE databases results showed that CMS1 and CMS4 colon cancer cells were less sensitive to OXA than CMS2 and CMS3 cells in terms of the sensitive cells proportion. Compared with, the expression of PGAM1 was higher in CMS1 and CMS4 cells than in CMS1 and CMS3 cells (P＜0. 05). HKB99 significantly inhibits the proliferation of SW480, SCUN2B and DLD-1 cells, with an IC50 of approximately 1μM. Annexin V/PI staining results showed that apoptosis of DLD-1 cells was significantly increased compared with Control group after HKB99 treatment (P＜0. 01). Results of CCK8 assay result showed that 1. 5μM HKB99 significantly enhanced the inhibitory effect of OXA on colon cancer DLD-1 cells compared with control group (IC50: 0. 37 vs 3. 26μM). The cooperativity index analysis result showed that the synergistic coefficient of OXA with HKB99 was less than 1 at the concentration between 1. 56μM and 25μM. Conclusions: In this study, we found that CMS1 and CMS4 colon cancer cells are less sensitive to OXA and higher level of PGAM1compared with CMS2 and CMS3 cells. An allosteric inhibitor of PGAM1, HKB99, enhances the sensitivity of colon cancer cells to OXA, which suggests that HKB99 may enhance the sensitivity of OXA chemotherapy and provide a potential treatment strategy for patients with individualized chemotherapy in colon cancer. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To probe into the improvement effects of compound Kushen injection combined with opioid analgesics on pain, quality of life, and coagulation function in patients with advanced colorectal cancer (CRC), and to explore the relevant mechanism of action by reviewing literature. METHODS: Totally 106 patients with advanced CRC admitted into the hospital from Jan. 2019 to Mar. 2024 were extracted to be divided into the monotherapy group (n = 53, treated with tramadol hydrochloride or oxycodone hydrochloride) and combination therapy group (n = 53, treated with compound Kushen injection combined with tramadol hydrochloride or oxycodone hydrochloride) via the random number table method. Visual Analogue Scale (VAS) scores, pain relief, quality of life (KPS score) and coagulation function (D-dimer and fibrinogen expression levels) were compared between two groups before and after treatment. RESULTS: Before treatment, there was no significant difference in VAS score, KPS score, D-dimer and fibrinogen expression levels between two groups (P > 0. 05). After treatment, the VAS score in the monotherapy group was (1. 28±1. 08) points, lower than (2. 72±0. 72) points in the combination therapy group; the degree of pain relief in the combination therapy group was significantly better than that in the monotherapy group, with statistically significant difference (P<0. 05). After treatment, the KPS score of combination therapy group was (85. 28± 11. 23) points, higher than (78. 87±12. 81) points of monotherapy group, the difference was statistically significant (P < 0. 05). After treatment, the expression levels of coagulation function indicators (D-dimer and fibrinogen) in monotherapy group were slightly higher than those before treatment, the difference was not statistically significant (P> 0. 05); the expression levels of coagulation function indicators of patients in the combination group was significantly lower than those before treatment, and lower than thos of the control group in the same period, the differences were statistically significant (P < 0. 05). CONCLUSIONS: The combination of compound Kushen injection and opioid analgesics is effective in relieving pain, improving quality of life and coagulation function in patients with advanced CRC. [ABSTRACT FROM AUTHOR]

Background and purpose: Rectal cancer occurs on the inner wall of the rectum, and metastasis-associated in colon cancer 1 (MACC1) can promote drug resistance in colon cancer cells. This study aimed to investigate the effect of MACC1 on oxaliplatin resistance in rectal cancer and its mechanism. Methods: Biosignal analysis of MACC1 and TCF7 expressions in rectal cancer tissues and signaling pathways enriched for MACC1 were carried out. The expressions of MACC1 and TCF7 in rectal cancer cells and rectal cancer oxaliplatin-resistant cells were detected by real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR), cell viability was detected by cell counting kit-8 (CCK-8), and cell proliferation was detected by cell colony formation assay. ECAR values, lactate production and glucose consumption were detected by Seahorse Biosciences XF96. Western blot was used to detect the expressions of glycolysis-related proteins. Dual luciferase reporter gene and ChIP were used to validate the regulatory relationship between MACC1 and TCF7. Normality test and homogeneity of variance analysis was performed on the data of each group by GraphPad Prism 8.0. If it conformed to normal distribution, one-way ANOVA or t-test would be used for inter group comparison, otherwise the comparison between groups would be conducted using Wilcoxon rank sum test. Using a two-sided test, P<0.05 was considered statistically significant. Results: MACC1 and TCF7 expressions were upregulated in rectal cancer, and knockdown of MACC1 significantly inhibited the viability of rectal cancer drug-resistant cells and the IC50 values of different concentrations of oxaliplatin treatments, as well as reduced the proliferation ability of rectal cancer oxaliplatin-resistant cells. Overexpression of MACC1 was able to promote the proliferation and glycolytic capacity of rectal cancer cells. Further studies revealed that the transcription factor TCF7 existed in the upper reaches of MACC1. Besides, this study analyzed the data from Cancer Genome Atlas Program (TCGA), and the result showed that knockdown of TCF7 was able to attenuate the promotional effect of overexpression of MACC1 on the glycolytic capacity and oxaliplatin resistance of rectal cancer cells. Conclusion: This study demonstrated that the TCF7/MACC1 axis could promote aerobic glycolysis and thus oxaliplatin resistance in rectal cancer cells. The findings suggest that targeting the TCF7/MACC1 axis or inhibiting the aerobic glycolysis pathway may be a novel therapeutic approach to inhibit oxaliplatin resistance in rectal cancer. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of docosahexaenoic acid (DHA) on human colon cancer cell line HT-29 and underlying mechanism. Methods Human colon cancer cell line HT-29 was incubated with DMSO (control), DHA (25, 50, 100 µmol/L) and 100 µmol/L DHA and/or 30 µmol/L 740Y-P. Proliferation was examined by MTT; apoptosis was detected by annexin V-FITC/PI. Western blot was used for detection of protein expression of Bcl-2, Bax apoptosis-related protein and PI3K/Akt/mTOR pathway, and RT-qPCR was used for checking mRNA expression of NLRP3/Caspase-1/IL-1ẞ pathway. Results Compared with the control group, DHA 25, 50, and 100 µmol/L treatment of HT-29 cells resulted in decreased cell survival (P < 0.05), increased apoptosis P < 0.05 ), decreased Bcl-2/Bax ratio P < 0.05 ) and decreased phosphorylation of PI3K, Akt and mTOR in HT-29 cells P < 0.05 or P < 0.01 . Expressions of NLRP3, Caspase-1 and IL-1ẞ mRNA were decreased (P < 0.05) . In addition, cell viability, protein phosphorylation (p-PI3K, p-Akt, p-mTOR) and relative mRNA expression of NLRP3, Caspase 1, and IL-1ẞ were lower in HT-29 cells which were co-incubated with DHA 100 µmol/L and 740Y-P 30 µmol/L than those in the control group ( P < 0.05 or P < 0.01 ) and 740Y-P 30 µmol/L group (P < 0.05), while higher than that of DHA 100 µmol/L group ( P < 0.05 or P < 0.01 ) . Conclusions DHA inhibits the proliferation of human colon cancer cell line HT-29, its mechanism is potentially related to the inhibition of PI3K/Akt/mTOR and NLRP3/Caspase-1/IL-1ẞ signaling pathways. [ABSTRACT FROM AUTHOR]

Objective: To study value of two-dimensional shear wave elastography(SWE) in the evaluation of antiangiogenic treatment effect of single colon cancer metastasis in liver of nude rat. Methods: Sixteen nude rats with colon cancer liver single metastasis were divided randomly into treatment group and control group. The treatment group was treated with Ramucirumab (8 mg/kg, tail vein injection) on Day 0, Day 4, Day 7 and Day 11 respectively, while the control group was injected with the same dose of saline. The tumor size and volume were measured before treatment (Day 0) and after 14 days of treatment (Day 14). On Day 14, to evaluate the stiffness of tumor and surrounding liver tissue, the liver tumor and surrounding liver tissue SWE examination were performed and the elastic parameters(including Vs-tumor, Vs-liver, E-tumor and E-liver) were measured and then the R-Vs (=Vs-tumor/Vs-liver) and R-E (= E-tumor/E-liver) were calculated respectively. Finally, expression of matrix metalloproteinase 2(MMP2) and transforming growth factor β2 (TGF β2) in tumors were detected by immunofluorescence staining. Results: There was no significant difference in the tumor size between the treatment group and the control group both on Day 0 and Day 14(P>0.05). Vs-liver and E-liver had no significant difference between the treatment group and the control group(P>0.05). Both Vs-tumor and E-tumor in treatment group were mildly higher than those in the control group, however, these differences were not statistically significant(P>0.05). In the treatment group, both R-Vs and R-E were significantly higher than those in the control group(P<0.05). The expression levels of MMP2 and TGFβ2 were significantly higher than those in control group respectively(P<0.05). Conclusion: The quantitative parameters of SWE may have the potential as an image biomarker indicating tumor stiffness for evaluating the anti-angiogenic therapy efficacy. [ABSTRACT FROM AUTHOR]

Objective The aim of this study was to investigate whether there are differences in the expression spectrums of RSK4 in different tumor cells and to predict the possible protein subtypes and their biological characteristics. Methods RNA was extracted from glioma cells GL261, ovarian cancer cells ID8, breast cancer cells 4T1 and 168FARN, colon cancer cells mc38 and CT26, gastric cancer cells MFC and lung cancer cells LLC1. The expressions and splicing isomers of RSK4 were detected by RT-PCR. The biological characteristics and functions of RSK4 were analyzed by bioinformatics. Results RT-PCR results showed that RSK4 was expressed in GL261, 4T1, mc38, CT26, MFC and LLC1; and multiple splicing isomers were expressed in different tumor cells. Open reading frame analysis revealed RSK4 may encode at least 11 protein subtypes. Secondary structure analysis showed that these protein subtypes encoded by the splicing isomers were composed of α-helix, extended strand, β-turn and random coil, and had the same conserved domain. The results of protein interaction network enrichment analysis showed that RSK4 exerted kinase activity in the nucleus and cytoplasm mainly through the mTOR signaling pathway and long-term potentiation. Conclusions RSK4 has different expression spectrums in different tumor cells, and may produces a variety of protein isoforms with different nitrogen terminals, which can be involved in different biological processes through multiple signaling pathways. [ABSTRACT FROM AUTHOR]

Objective: To discuss the effect of sialic acid-binding immunoglobulin-like lectin-15(Siglec15) derived from M2 tumor-associated macrophages (M2-TAMs) on promoting the malignant biological behavior of the esophageal squamous cell carcinoma (ESCC) through bioinformatics analysis, and to validate the findings through cell experiment. Methods: The Tumor Immune Estimation Resource (TIMER) online Database was used to analyze the expression differences and immune infiltration of Siglec15 in pan-cancer and adjacent normal tissues. Real-time fluorescence quantitative PCR (RT-qPCR) method was used to detect the expression levels of Siglec15 mRNA in M2-TAMs and ESCC EC109 and KYSE150 cells. Based on the non-contact co-culture of M2-TAMs and ESCC cells, the following groups were set up，such as EC109/KYSE150 group, EC109/KYSE150+si-NC group (transfected with si-NC sequence), and EC109/KYSE150+si-Siglec15 group (transfected with si-Siglec15#1 and si-Siglec15#2 sequences). CCK-8 method was used to detect the proliferation activities of the cells in various groups; wound healing assay was used to detect the wound healing rates of the cells in various groups; Transwell chamber assay was used to detect the numbers of migration and invasion cells in various groups; flow cytometry was used to detect the apoptotic rates of the cells in various groups. Results: The bioinformatics analysis results showed that compared with adjacent normal tissue, the expression levels of Siglec15 mRNA in pan-cancer tissues such as esophageal cancer, colon cancer, and head and neck squamous cell carcinoma tissues were increased (P<0. 05 or P<0. 01), and the expression level of Siglec15 mRNA in esophageal cancer tissue was significantly positively correlated with the infiltration of the macrophages (P<0. 05). Compared with the EC109 cells and KYSE150 cells, the expression level of Siglec15 mRNA in M2-TAMs was significantly increased (P<0. 01). There was no significant difference in the proliferation rate of the cells among EC109/KYSE150 group, EC109/KYSE150+si-NC group, and EC109/KYSE150+si-Siglec15 group(P>0. 05). Compared with EC109/KYSE150 group, after treated for 24 and 48 h, the wound healing rate of the cells in EC109/KYSE150+si-NC group was increased (P<0. 01), the numbers of migration and invasion cells were increased (P<0. 05), and the apoptotic rate was decreased (P<0. 01). Compared with EC109/KYSE150+si-NC group, the wound healing rates of the cells in EC109/ KYSE150+si-Siglec15#1 group and EC109/KYSE150+si-Siglec15#2 group were decreased (P< 0. 05), the numbers of migration and invasion cells were decreased (P<0. 05), and the apoptotic rates of the cells had no significant difference (P>0. 05). Conclusion: Siglec15 derived from M2-TAMs may be a key factor in promoting the migration and invasion of the ESCC cells. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effects of isoliensinine (Iso) on the proliferation, apoptosis and autophagy of colon cancer SW480 cells through PI3K/Akt/mTOR signaling pathway. Methods: Colon cancer SW480 cells were treated with 10, 20 and 40 μmol/L Iso, and the effects of Iso on the cell proliferation capacity, apoptosis and expressions of autophagy related proteins LC3 I, LC3II and p62 were detected by CCK-8, flow cytometry and Western blot, respectively. Then, SW480 cells were treated respectively with 20 μmol/L Iso and 25 μmol/L PI3K activator 740 Y-P, and the cells were divided into the control group, the 740 Y-P group, the Iso group and the Iso+740 Y-P group. The effects of 740 Y-P on the apoptosis and the expressions of LC3 I, LC3 II, p62, PI3K, p-PI3K, mTOR and p-mTOR proteins in each group were detected by flow cytometry and WB. Results: After treatments with 10, 20 and 40 μmol/L Iso, the proliferation capacity of SW480 cells was decreased significantly (all P<0.05); the apoptosis rate was increased significantly (all P<0.05); the expressions of LC3 II/LC3 I were up-regulated significantly (all P<0.05), and the expression of p26 protein was down-regulated significantly (all P<0.05). After treatments with Iso and 740 Y-P, compared with the control group, the apoptosis rate and LC3 II/LC3 I expression of the 740 Y-P group were decreased significantly (both P<0.05), while the expressions of p26, p-PI3K/PI3K and p-mTOR/mTOR were increased significantly (all P<0.05).The apoptosis rate and LC3 II/LC3 expression in the Iso group were increased (both P<0.05) and the expressions of p26, p-PI3K/PI3K and p-mTOR/mTOR were decreased (all P<0.05). Compared with the 740 Y-P group, the apoptosis rate and LC3 II/LC3 I expression were increased in the Iso+740 Y-P group (P<0.05), while the expressions of p26, p-PI3K/PI3K and p-mTOR/mTOR were decreased (all P<0.05). Compared with the Iso group, the apoptosis rate and LC3 II/LC3 I expression were decreased (both P<0.05), and the expressions of p26, p-PI3K/PI3K, and p-mTOR/mTOR were increased significantly (all P<0.05) in the Iso+740 Y-P group. Conclusion: Iso inhibits the proliferation and induces the apoptosis and autophagy of SW480 cells by inhibiting PI3K/Akt/mTOR signaling pathway. [ABSTRACT FROM AUTHOR]

Objective: To investigate therapeutic effect of reinfusion of tumor-infiltrating lymphocyte (TIL) with clustered regularly interspaced short palindromic repeats/CRISPR-associated 9(CRISPR/CAS9) knockout programmed death-1( PD-1) on colon cancer in mice. Methods: Subcutaneous injection of CT26 was used to establish mouse colon cancer model. TIL was extracted from tumor tissue of three model mice, and peripheral blood lymphocytes were extracted. PD-1 gene was knocked out of TIL. Reinfusion experiments were divided into control group (Control), lymphocyte group (Lym), tumor-bearing mouse TIL group (TIL), lentivirus empty empty group (pVSV-G-PX458-NC) and PX458-PD-1-sgRNA1 group (PD-1-sgRNA1), with 10 mice in each group. Tumor tissue quality and tumor inhibition rate were detected in each group. TUNEL was used to detect cell apoptosis in tumor tissues of mice. ELISA was used to detect contents of TNF-α and IFN-γ in tumor tissues of mice. Immunohistochemistry was used to detect expressions of CD4+T and CD8+T cells in tumor tissue. Immunofluorescence was used to detect expressions of proliferating cell nuclear antigen-67 (Ki-67) and vascular endothelial growth factor (VEGF). Western blot was used to detect expressions of PD-1 and its ligand PD-L1 in tumor tissues. Results: PD-1-sgRNA1 could significantly inhibit growth of mouse tumor cells in vivo, inhibit expressions of Ki-67 and VEGF in tumor tissues, as well as expressions of PD-1 and PD-L1, elevate apoptosis rate, contents of TNF-α and IFN-γ in tumor tissues, and expressions of CD4+T and CD8+T cells (all P<0.05). Conclusion: Reinfusion of TIL with CRISPR/CAS9 knockout PD-1 can significantly inhibit expressions of Ki-67 and VEGF in colon cancer mice, enhance infiltration of CD4+T and CD8+T cells, induce tumor cell apoptosis and inhibit tumor growth. [ABSTRACT FROM AUTHOR]

Background and purpose: According to current consensus, adverse high-risk pathological features are only associated with adjuvant therapy for stage II colorectal cancer (CRC). As important prognostic factors, we further explored the possibility of identifying patients with potential recurrence and poor prognosis based on these incorporating high-risk pathological features. Methods: This is a cohort study. A retrospective analysis was conducted on clinical data of CRC patients who underwent surgical treatment at the Second Department of Colorectal Surgery, Fudan University Affiliated Shanghai Cancer Center from 2008 to 2018. This study was approved by the Ethics Committee of the Fudan University Shanghai Cancer Center (approval No.: 050432-4-2108*), and the study complies with the Declaration of Helsinki. A total of 9 875 patients were enrolled, including 5 859 males and 4 016 females, aged [M (IQR)] 60 (16) years (range: 16 to 94). Median follow-up time was 1 779.0 days [95% CI: 1 750.1-1 807.9]. We used the Kaplan-Meier method to plot survival curves for different groups. Cox multivariate analysis was used to identify independent risk factors for 5-year overall survival (OS), disease-free survival (DFS) and recurrence-free survival (RFS). Finally, a column chart model was constructed to evaluate and stratify patient prognosis. The Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) checklist was followed for this cohort study. Results: According to the number of incorporating high-risk pathological features, patients were divided into five groups: Hr_0 group (0 incorporating high-risk pathological feature), Hr_1 group (1 incorporating high-risk pathological feature), Hr_2 group (2 incorporating high-risk pathological features), Hr_3 group (3 incorporating high-risk pathological features), and Hr_4 group (4 or more incorporating high-risk pathological features). The Kaplan-Meier survival curve results indicated significant differences in OS, DFS and RFS among different groups (all P<0.001). Subgroup analysis was conducted on stage II colorectal cancer, and the survival curves of OS, DFS and RFS in different Hr groups overlapped with each other. Compared to the overall population, the survival differences in different groups were significantly reduced, indicating that stage II colon cancer patients with incorporating high-risk pathological features may benefit from adjuvant chemotherapy. The independent prognostic factors for RFS included age, pT stage, pN stage and Hr group. The survival curves of OS, DFS and RFS indicated that the prognosis of Hr_4 group was significantly worse than that of stage IIIc patients; 5.2% and 14.1% of stage I and II patients had two or more incorporating high-risk pathological features (Hr group≥2), respectively. Finally, a column chart model was constructed by incorporating the independent prognostic risk factors for CRC mentioned above. The calibration curve showed a good consistency between the actual observations and the predictions made by the nomogram, and the decision curve analysis (DCA) indicated that the model constructed in this study had good efficacy in stratifying recurrence. Conclusion: The number of incorporating high-risk pathological features is an independent prognostic factor for RFS in patients with stage I-III CRC. Combining it as a multiclass variable with age, pT and pN stage has good prognostic stratification and recurrence stratification efficacy, which is expected to guide clinical treatment. [ABSTRACT FROM AUTHOR]

Objective To identify small molecule inhibitors of APC-mutant colon cancer and provide lead compounds for targeted therapy of colon cancer. Methods APC-mutant colon cancer cell lines that stably express 7*Tcf-GFP/SV40-Cherry (7TGC) dual fluorescence reporter system was constructed for small- molecule inhibitor screening. Cell viability, colony formation, EdU incorporation, and xenograft tumor assay were used to evaluate the inhibitory effect of these inhibitors on APC-mutant colon cancer in vitro and in vivo. Western blot and co-immunoprecipitation assays were used to explore the molecular mechanism. Results Four small molecules that inhibited Wnt activity in APC-mutant colon cancer cells were discovered. Shikonin exhibited significant inhibition of cell viability and proliferation while inducing apoptosis of APC-mutant colon cancer cells. Xenograft tumor assay demonstrated that shikonin significantly reduced tumor growth in vivo. Furthermore, Western blot and co-immunoprecipitation assays revealed that shikonin markedly decreased ẞ-catenin levels. Conclusion Shikonin effectively inhibits Wnt activity and suppresses tumor growth in APC-mutant colon cancer. [ABSTRACT FROM AUTHOR]

Theaflavin is a high-quality component of black tea, which has good medical and health functions. Highspeed countercurrent chromatography (HSCCC) has been applied for the separation of theaflavins and catechins, and examined the cytotoxic activity of the individual theaflavins against human liver cancer (HepG2) cells, Colonic adenocarci-noma(Caco-2)cells. Six components were separated and prepared by HSCCC. Further analysis of these compounds by HPLC indicated that that each component F4 contains theaflavin (TF), F5 contains theaflavin-3-gallate (TF-3-G) and theaflavin-3'-gallate (TF-3'-G), and F6 contains theaflavin-3, 3'- gallate (TFDG). The results show TFDG was selected to study the inhibitory effect on cancer cells. CCK-8 was used to assess cell proliferation. TFDG has a significant inhibitory effect on HepG-2 and Caco-2 cells in a time-dependent and dose-dependent manner with the increase of concentration and time. It found a solvent system for the preparation of theaflavins in large quantities was selected based on the partitioning coefficient K and separation factor a. Also, we acknowledged that there is a certain relationship between cancer prevention and quinone reductase (QR). Combining experimental data with theory, by linking molecular docking technology was used to verify that TFDG and QR can form stable complexes, It also inducing QR activity can enhance the anticancer effect, it can providing a basis for further research on the effect of theaflavin on cancer cells. Keywords high speed countercurrent chromatography; hepatoma cells; colon adenocarcinoma cells; molecular docking [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To explore the risk factors for the occurrence of anastomotic fistula after radical right hemicolectomy, and to further assess the predictive efficacy of related factors. Methods A total of 467 patients who underwent radical right hemicolectomy for colon cancer at Jiangmen Central Hospital from January 2020 to January 2024 were retrospectively included and grouped according to the occurrence of anastomotic fistula in the postoperative period. Independent risk factors for the occurrence of anastomotic fistula after radical right hemicolonic cancer were analyzed by univariate and multivariate methods, and the predictive efficacy of the various factors on the risk of anastomotic fistula after the surgery was assessed by receiver operating characteristic (ROC) curve. Results Fifty cases of anastomotic fistula occurred after surgery in 467 patients included in this study, with an incidence rate of 10.71%. The results of multifactorial logistic regression analysis showed that the maximum diameter of the tumor＞5 cm, the Nutritional Risk Screening 2002 (NRS2002) score≥3, and the postoperative albumin level＜30 g/L were the independent risk factors for the occurrence of anastomotic fistula after right hemicolectomy (P＜0.05). The ROC curve analysis results showed that the maximum diameter of the tumor, NRS2002 score, postoperative albumin level and the predicted probability of the regression model for the risk of anastomotic fistula after radical right hemicolectomy were 0.63, 0.71, 0.68, 0.88, respectively. Conclusion The occurrence of anastomotic fistula after radical right hemicolectomy may be related to the maximum diameter of the tumor, the NRS2002 score and the postoperative albumin level, and the construction of a regression model based on the above risk factors can accurately predict the risk of postoperative anastomotic fistula.

Objective To analyze the current status of drug compliance and influencing factors of oral anti-tumor targeted drugs in elderly patients with colon cancer after discharge. Methods A total of 110 elderly patients with colon cancer admitted to the First Affiliated Hospital of Harbin Medical University from February 2022 to February 2023 were selected.All patients received oral anti-tumor targeted drug therapy after discharge.Morisky medication compliance questionnaire was used to assess medication compliance, and then the factors affecting medication compliance were statistically analyzed. Results A total of 34 patients had good compliance(good compliance group) and 76 patients had poor compliance (poor compliance group).Univariate analysis showed that the proportion of lack of social support, adverse reactions to oral targeted drug therapy, adverse psychological reactions, poor economic conditions, and lack of knowledge of oral targeted drug therapy in the poor compliance group was significantly higher than that in the good compliance group, and the differences were statistically significant(P

Objective: To explore the expression and significance of arachidonate 12⁃lipoxygenase (ALOX12) in cancer tissues of colon cancer patients. Methods: Tumor and peritumoral tissues of 257 colon cancer patients were retrospectively collected, and the expression of ALOX12 was detected by immunohistochemistry (IHC) to compare the differences in expression within the tumor and peritumoral tissues, and the relationship between ALOX12 expression and clinicopathological features of colon cancer was analyzed. The 5⁃year overall survival (OS) of the patients was analyzed using Kaplan⁃Meier curves, and the factors affecting the 5⁃year OS of the patients were investigated by univariate and multivariate Cox regression analyses. Results: ALOX12 was more positively expressed in tumors compared to peritumoral tissues (63.8% vs. 33.1%), and the difference was statistically significant (P < 0.001). The expression of ALOX12 was not significantly correlated with the patient’s age, gender, and tumor site (P > 0.05), but was strongly correlated with TNM staging and lymph node metastasis (P < 0.05). Five⁃year OS of patients with high expression of ALOX12 was markedly lower than those patients with low expression of ALOX12 (P < 0.001). Single variable and multivariate Cox analyses indicated that age, TNM staging, lymph node metastasis, and ALOX12 expression were independent factors influencing the 5-year OS rate (P < 0.05). Conclusion: High expression of ALOX12 is associated with TNM staging and lymph node metastasis of colon cancer, which can serve as a biomarker to predict the patient’s condition and prognosis. [ABSTRACT FROM AUTHOR]

Copyright of Practical Oncology Journal is the property of Journal of Practical Oncology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To investigate the relationship between the expression of long-chain non-coding ribonucleic acid (LncRNA）lymphocytic leukemia deletion gene 1 (DLEU1) and LncRNA NONHSAT017458 in colon cancer tissues and clinicopathological features and prognosis. Methods: 136 colon cancer patients who were admitted to our hospital from March 2020 to December 2022 were selected,the expression of LncRNA DLEU1 and LncRNA NONHSAT017458 was detected in surgically resected cancer tissues and cancer adjacent tissues (more than 5 cm from the cancer adjacent tissues）. The expression differences of LncRNA DLEU1 and LncRNA NONHSAT017458 in colon cancer tissues with different pathological features were compared, the survival rate of colon cancer patients with different LncRNA DLEU1 and LncRNA NONHSAT017458 expression were analyzed by Kaplan-Meier survival curve, the difference of survival rate were tested by Log-Rank test, the factors affecting the survival of colon cancer patients were analyzed by univariate and multivariate Cox risk proportional regression analysis. Results: The expression of LncRNA DLEU1 and LncRNA NONHSAT017458 in cancer tissues was higher than that in cancer adjacent tissues, and the difference was statistically significant (P＜0.05）.The expression of LncRNA DLEU1 and LncRNA NONHSAT017458 in cancer tissues with tumor diameter≥4 cm, low differentiation,T3-4and N1-2was higher than that in tumor diameter＜4 cm, medium and high differentiation, T1-2and N0, and the difference was statistically significant (P＜0.05）. The 3-year overall survival (OS) rate and 3-year progression-free survival (PFS) in colon cancer patients with high expression of LncRNA DLEU1 and LncRNA NONHSAT017458 were lower than those in colon cancer patients with low expression of LncRNA DLEU1 and LncRNA NONHSAT017458, and the differences were statistically significant (P＜0.05）. Multivariate Cox regression analysis showed that high T stage, high N stage, high LncRNA DLEU1 expression, and high LncRNA NONHSAT017458expression were risk factors for poor prognosis in colon cancer patients (P＜0.05）. Conclusion: The expression of LncRNA DLEU1 and LncRNA NONHSAT017458 is up-regulate in colon cancer tissues, the high level of expression is relate to the high T, N stage and poor differentiation of colon cancer, which can lead to adverse outcomes in patients. [ABSTRACT FROM AUTHOR]

Objective To determine the causal relationship between acromegaly and colon cancer by using two-sample Mendelian randomization. Methods Genetic loci closely related to acromegaly in the whole genome-wide association study (GWAS) were selected as tool variables, and the genetic data of colon cancer from different GWASs were analyzed by two-sample Mendelian randomization (MR).The inverse variance weighting method (IVW) of the random effect model was used for analysis, and MR-weighted median and MR-Egger methods were used to supplement the analysis. Results were presented as OR values. Results Four SNPs closely related to acromegaly were obtained as tool variables, and the multiplicity test of tool variables showed that P=0.59.Three methods were used to estimate causal effects.The IVW analysis were OR=1.00(0.99-1.001) and P=0.42;the MR-Egger analysis results were OR=1.00(0.99-1.001) and P=0.42;and the Weighted median analysis results were OR=1.00(1.00-1.001) and P=0.03.The sensitivity test showed that the confidence interval of the tool variable SNP passed through 0, indicating the robustness of the MR results. Conclusion Acromegaly is not an independent risk factor for colon cancer.

Objective To investigate the expression of UBQLN2 gene in colon cancer and its immunoregulatory function. Methods Colon cancer and their matched paracancer tissues surgically removed in the First Affiliated Hospital of Hebei North University from January 2021 to June 2023 were collected. The expression of UBQLN2 was detected by transcriptome sequencing, the expression level of UBQLN2 mRNA was detected by qRT⁃PCR, and the expression of UBQLN2 protein was detected by immunohistochemical. The relationship between the expression of UBQLN2 and the clinical pathological characteristics and prognosis of colon cancer patients was analyzed. Multicolor immunofluorescence was used to detect the co⁃expression of UBQLN2 and TGF⁃β. Single⁃cell transcriptome sequencing and TCGA database were used to verify the expression of UBQLN2 in colon cancer and its relationship with immunosuppressive factors, TGF⁃β and prognosis of colon cancer. Results Transcriptome analysis showed that UBQLN2 gene was significantly overexpressed in colon cancer tissues, and its mRNA expression level was higher than that in cancer⁃adjacent tissues (P<0.01). The relative expressions of UBQLN2 mRNA in 275 colon cancer tissues and 41 paracancer tissues which collected from TCGA database were also significantly higher in colon cancer tissues than that in cancer ⁃adjacent tissues (P<0.001). Immunohistochemical results showed that UBQLN2 was mainly expressed in the cytoplasm, and the positive expression intensity of UBQLN2 protein in colon cancer tissues was obviously higher than that in cancer⁃adjacent tissues. The results of qRT⁃PCR showed that UBQLN2 mRNA expression in colon cancer tissues was significantly higher than that in cancer ⁃adjacent tissues (P<0.001). Pathway enrichment analysis showed that the tumor proliferation pathway was significantly up⁃regulated, and the immune activation pathway was significantly down⁃regulated in the UBQLN2 high expression group. Moreover, compared with UBQLN2 low expression group, UBQLN2 high expression group had higher immune escape score (P<0.05), lower expression of CD8+ T cell specific markers, smaller immune recruitment factors and immune killer factors (all P<0.05), and higher expression of immune depletion molecules (all P<0.05). The expressions of TGF⁃β, IL10, ARG1 and other immunosuppressive cytokines in UBQLN2 high expression group were higher than those in UBQLN2 low expression group (all P<0.05), and UBQLN2 was positively correlated with TGF⁃β expression (r=0.280, P<0.0001); UBQLN2 and TGF⁃β were co⁃expressed in tumors. Patients with both high expression of TGF ⁃β and UBQLN2 had worse prognosis than those with both low expression (P=0.004). Single ⁃ cell transcriptome sequencing showed that colon cancer with high expression of UBQLN2 was highly expressed TGF⁃ β and the microenvironment was immuno⁃ suppressed. Conclusions UBQLN2 is highly expressed in colon cancer and associated with poor prognosis. Colon cancer with high expression of UBQLN2 may inhibit the killing activity of CD8+T cells by releasing TGF ⁃ β cytokines and realizing immune escape. UBQLN2 may be a potential molecular target for the treatment of colon cancer. [ABSTRACT FROM AUTHOR]

Objective Exploring the mechanism of Qizhu Kangai Formula in regulating the key protein of protein tyrosine phosphatase 1B (PTP1B) of homo-heterologous adhesion crosstalk inhibition of colon cancer metastasis. Methods Prepare blank serum and Qizhu Kangai Formula containing serum. Analysis of effective chemical components in serum containing Qizhu Kangai Formula using liquid chromatography-mass spectrometry technology. Constructing PTP1B overexpression model(OE-PTP1B HCT116) in vitro through phasmid transfection. After detecting the cell survival rate of OE-PTP1B HCT116 using CCK-8 method, select 20% medicated serum and 5%, 10%, 20% Qizhu Kangai Formula containing serum. Scratch assay, transwell assay, and adhesion assay were used to detect the migration, invasion, and adhesion of cells overexpressing PTP1B, respectively. Western blotting was used to detect protein expression level of PTP1B, vinculin, E-cadherin, integrin αν subunit and integrin β3 subunits. Results Liquid chromatography-mass spectrometry analysis revealed that the serum of Qizhu Kangai Formula contains 12 main effective chemical components. Among them, the highest content is Calycosin-7-glucoside. The expression levels of PTP1B and vinculin proteins were increased (P<0.05), indicating the successful construction of the model. Compared with the blank serum group, the survival rate of cells overexpressing PTP1B was decreased in different volume fractions of Qizhu Kangai Formula containing serum groups (P<0.05). Compared with the blank serum group, the wound healing rate of cells in the 10% and 20% Qizhu Kangai Formula containing serum groups decreased, the number of invasive cells in each containing serum group decreased, the number of HCT116 cells adhering to cells in each Qizhu Kangai Formula containing serum group increased, the number of HCT116 cells adhering to the matrigel decreased. Compared with the blank serum group, the expression level of E-cadherin protein was increased(P<0.05), the expression level of PTP1B, vinculin, integrin αν subunit, and integrin β3 subunit were reduced in the 20% Qizhu Kangai Formula containing serum group. Conclusion The mechanism of Qizhu Kangai Formula in inhibiting colon cancer metastasis may be related to the regulation of homo- and hetero-adhesion crosstalk mediated by PTP1B. [ABSTRACT FROM AUTHOR]

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Objective　To investigate the expression level of miR-218-5p and LAYN in colon cancer and the effects of their regulatory relationship on the progress of colon cancer. Methods RT-qPCR was used to detect the expression of miR-218-5p in colon cancer tissues, adjacent tissues, and cell lines. Western blot was used to detect the expression level of LAYN protein in colon cancer tissues, adjacent tissues, and cell lines. The in situ hybridization（ ISH） was used to detect the expression of miR-218-5p in colon cancer and adjacent tissues. Immunohistochemical（IHC） experiment was used to detect the distribution and expression of LAYN protein in colon cancer tissues and adjacent tissues. The dual luciferase experiment was used to detect the binding relationship between miR-218-5p and 3'- rn-translation region（ UTR） of LAYN. CCK-8 was used to detect the cell proliferation. Transwell was used to detect the invasion ability of cells. The flow cytometry was used to detect the apoptosis level of cells. Western blot was used to detect the expression level of cleaved Caspase3 in cells. Results The expression of miR-218-5p decreased in colon cancer tissues and colon cancer cell lines， with the lowest expression in HT-29 cells（P < 0.000 1），and the expression of LAYN increased and the highest expression in HT-29 cells（ P < 0.05） . The double luciferase reporter gene experiment（ P < 0.01） combined with Western blot experiment（P < 0.01） showed that miR-218-5p could bind to the 3'UTR region of LAYN and inhibit its protein expression. In cell experiments， overexpression of miR-218-5p inhibited cell proliferation（ P < 0.05） ， invasion（P < 0.001），and increased apoptosis（P < 0.01），and the expression of cleaved Caspase3 protein（P < 0.01）. Overexpression of LAYN promoted cell proliferation（P < 0.05），invasion（P < 0.001），and decreased apoptosis（P < 0.000 1） and the expression of cleaved Caspase3 protein（ P < 0.01），while overexpression of miR-218-5p and LAYN partially reversed the above changes. Conclusion　The expression level of miR-218-5p is decreased in colon cancer tissues. Cell experiments show that miR-218-5p inhibits cell invasion and proliferation and promotes cell apoptosis through targeted regulation of LAYN. [ABSTRACT FROM AUTHOR]

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Objective To screen the potential key genes associated with colon cancer(CC) by bioinformatics analysis based on Gene Expression Omnibus (GEO) database, and verify them through in vitro experiments to explore potential colon cancer molecular markers. Methods The human CC data sets GSE10950 and GSE74602 were obtained from GEO database. The differentially expressed genes (DEGs) in colon cancer and adjacent tissues were screened by GEO2R tool and Venn diagram software. DEGs were used to perform by Gene Ontology(GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). The Protein-Protein Interaction (PPI) network of DEGs was constructed by STRING database, then the key genes were screened with Cytoscape software. GEPIA database was used to validate expression and prognostic value of key genes. Finally, the functions of key genes were further verified by cell transfection and CCK8 assays. Results 515 DEGs were obtained from two datasets, of which 223 were up-regulated and 292 were down-regulated. GO enrichment analysis showed that up-regulated DEGs were mainly involved in negative regulation of cell cycle, transcriptional control. KEGG signaling pathways analysis showed that up-regulated DEGs were mainly enriched in cell cycle signaling pathways. A total of 33 hub genes were screened through the PPI. UCLCAN analysis was implemented and 7 of 33 genes were relative to lower survival rate of CC patients. The expression levels of 7 genes by GEPIA analysis (P＜0.05).It was verified by GEPIA database that CCNB1,CCNA2,CDC20,CDKN3,DLGAP5,HMMR and NCAPG were highly expressed in colon cancer tissues. KEGG pathway enrichment and found that three critical genes (CCNB1, CDC20 and CCNA2) enriched in cell cycle pathway. The inhibition of CCNB1,CDC20 or CCNA2 significantly promoted proliferation of colon cancer cells. Conclusions A total of 7 key genes were identified to be involved in the occurrence of CC. The expression of CCNB1,CDC20 and CCNA2 is potentially related to the poor prognosis in CC, which may be potential targets of clinical treatment and prognostic markers for CC patients.

Objective To investigate the impacts of pachymic acid (PA) on proliferation and apoptosis of human colon cancer cell line (HT-29) and its potential mechanism. Methods The cells were divided into blank group, 20, 40 and 80 μmol/L PA groups. The proliferation of HT-29 cells was detected by MTT method; The cell cycle and apoptosis of HT-29 cells were detected by flow cytometry; The expression of cell cycle, apoptosis and Akt/MDM2/p53 signal pathway related proteins in HT-29 cells were detected by Western blot. The tumor xeno-transplantation model with HT-29 cells was constructed, and then the tumorigenic nude mice were randomly divided into control group, intra-peritoneal injection of 10, 30 and 60 mg/kg PA groups(6 in each group), the tumor volume and weight were measured; The expression of Ki-67 and of cleared caspase-3 proteins in tumor tissue was detected by immuno-histochemistry; The expression of Akt/MDM2/p53 signal pathway related protein in tumor tissue was detected by Western blot. Results PA of all doses obviously inhibited proliferation of HT-29 cells, the proportion of cells in S phase and in G2/M phase was deceased and the expression of B cell lymphoma gene-2(Bcl-2), cyclin D1, cycle protein dependent activating enzyme 2(CDK2) proteins all decreased, The ratios of p-Akt/Akt and p-MDM2/MDM2 in a concentration-dependent manner increased(P＜0.05).The apoptosis rate, the ratio of cells in G0/G1 phase and the protein expression of Bax, cleaved caspase-3 and p53 also increased(P＜0.05). PA in all dose groups obviously reduced the tumor volume, weight, the expression of Ki-67 protein and the ratios of p-Akt/Akt, p-MDM2/MDM2 in tumor tissue of nude mice (P＜0.05), and increased the protein expression of cleaved caspase-3 and p53 in tumor tissue(P＜0.05). Conclusions PA can induce apoptosis and cell cycle arrest of colon cancer cells and inhibit cell proliferation. Its mechanism may be related to the regulation of Akt/MDM2/p53 signal pathway.

To summerize the effect of moxibustion therapy and nursing interventions on the peripheral neuropathic pain of lower limbs caused by oxaliplatin. A comprehensive pain assessment was conducted for the establishment of following nursing plan. The combination treatment of moxibustion and acupoint massage was carried out to relive the peripheral neuropathic pain of lower limbs and ensure the completion of chemotherapy. (本文总结1例艾灸疗法缓解奥沙利铂致下肢周围神经病变性疼痛的护理经验。评估患者疼痛程度, 明确干预方案, 先用生姜涂擦, 再用艾灸条艾灸下肢, 并进行穴位按摩。通过肿瘤绿色调护, 有效减轻患者下肢周围神经病变性疼痛, 保障化疗的顺利进行, 对提高患者生存质量具有积极意义。)

To explore the experience of multidisciplinary team collaboration in the treatment and postoperative nursing of a patient with colon cancer. According to the characteristics of the patient's disease, multidisciplinary consultation was used to formulate the operation plan preoperatively. The nursing group also organized various professional teams to conduct nursing evaluation, formulated the corresponding nursing plan, and provided professional and standardized nursing interventions on body position management, catheter maintenance, nutrition support and exercise guidance. The multidisciplinary team model can accelerate the postoperative rehabilitation process of the patient with colon cancer (本文总结1例结肠癌手术患者多学科团队协作护理体会。针对患者疾病特点, 采用多学科联合会诊制定手术方案和护理措施, 术前完善检查、做好宣教, 术后给予体位护理、管路护理、营养指导、锻炼指导等护理干预, 以加速患者康复并提高患者满意度。)

Laparoscopic resection of colon cancer in the elderly is one of the common surgical operations, but hypothermia during operation is very harmful to elderly patients undergoing laparoscopic colon cancer surgery. Even the occurrence of mild hypothermia will cause significant damage to patients. This article reviews studies about the effect of hypothermia on the elderly patients, the causes of hypothermia and perioperative nursing measures, and provide reference for improving perioperative nursing quality and surgical safety of laparoscopic resection of colon cancer in the elderly. (老年腹腔镜结肠癌切除术是外科常见的手术之一, 但术中低体温会对老年患者手术安全造成严重影响, 即便是轻度低体温的发生, 也会给患者造成不可忽视的损伤。本文针对低体温对机体的影响、发生的原因及围手术期护理措施进行综述, 旨在为提升腹腔镜结肠癌切除围手术期护理质量和确保老年患者手术安全提供参考。)

Objective To investigate the demand of the continuous health management network platform for patients after endoscopic treatment of colorectal polyps, and to provide theoretical basis for the building of a continuous health management network platform for patients after endoscopic treatment of colorectal polyps in the future. Methods Objective sampling method was used to select 168 patients who underwent endoscopic treatment for colorectal polyps in the Department of Gastroenterology of a third-class A hospital in Luzhou City as the research objects. General data questionnaire and the network platform continuous nursing knowledge demand questionnaire were used to investigate them, and descriptive statistics were carried out. Results Among the patients surveyed, 158 cases (94.05%) thought that postoperative network platform was needed. More inclined to establish WeChat group in 52 cases (30.95%), WeChat public official account in 79 cases (47.02%) were, APP in 23 cases (13.69%), applet in 9 cases (5.36%) and health website in 5 cases (3.00%). Patients with different characteristics of rectal polyps after operation have the lowest demand for continuous nursing knowledge on network platform (33.60±0.89) and the highest demand for continuous nursing knowledge (35.80±1.62), both of which are at a high level. Conclusion Patients after endoscopic treatment of colorectal polyps have a high demand for continuous health management network platform. Relevant departments should build a comprehensive and systematic continuous health management network platform based on patients′ needs to reduce postoperative complications and improve patients′ satisfaction. [ABSTRACT FROM AUTHOR]

Objective To investigate the impacts of pachymic acid (PA) on proliferation and apoptosis of human colon cancer cell line (HT-29) and its potential mechanism. Methods The cells were divided into blank group, 20, 40 and 80 μmol/L PA groups. The proliferation of HT-29 cells was detected by MTT method; The cell cycle and apoptosis of HT-29 cells were detected by flow cytometry; The expression of cell cycle, apoptosis and Akt/MDM2/p53 signal pathway related proteins in HT-29 cells were detected by Western blot. The tumor xeno-transplantation model with HT-29 cells was constructed, and then the tumorigenic nude mice were randomly divided into control group, intra-peritoneal injection of 10, 30 and 60 mg/kg PA groups (6 in each group), the tumor volume and weight were measured; The expression of Ki-67 and of cleared caspase-3 proteins in tumor tissue was detected by immuno-histochemistry; The expression of Akt/MDM2/p53 signal pathway related protein in tumor tissue was detected by Western blot. Results PA of all doses obviously inhibited proliferation of HT-29 cells, the proportion of cells in S phase and in G2/M phase was deceased and the expression of B cell lymphoma gene-2 (Bcl-2), cyclin D1, cycle protein dependent activating enzyme 2 (CDK2) proteins all decreased, The ratios of p-Akt/Akt and p-MDM2/MDM2 in a concentration-dependent manner increased (P＜0.05).The apoptosis rate, the ratio of cells in G0/G1 phase and the protein expression of Bax, cleaved caspase-3 and p53 also increased (P＜0.05). PA in all dose groups obviously reduced the tumor volume, weight, the expression of Ki-67 protein and the ratios of p-Akt/Akt, p-MDM2/MDM2 in tumor tissue of nude mice (P＜0.05), and increased the protein expression of cleaved caspase-3 and p53 in tumor tissue (P＜0.05). Conclusions PA can induce apoptosis and cell cycle arrest of colon cancer cells and inhibit cell proliferation. Its mechanism may be related to the regulation of Akt/MDM2/p53 signal pathway. [ABSTRACT FROM AUTHOR]

Objective To screen the potential key genes associated with colon cancer (CC) by bioinformatics analysis based on Gene Expression Omnibus (GEO) database, and verify them through in vitro experiments to explore potential colon cancer molecular markers. Methods The human CC data sets GSE10950 and GSE74602 were obtained from GEO database. The differentially expressed genes (DEGs) in colon cancer and adjacent tissues were screened by GEO2R tool and Venn diagram software. DEGs were used to perform by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). The Protein-Protein Interaction (PPI) network of DEGs was constructed by STRING database, then the key genes were screened with Cytoscape software. GEPIA database was used to validate expression and prognostic value of key genes. Finally, the functions of key genes were further verified by cell transfection and CCK8 assays. Results 515 DEGs were obtained from two datasets, of which 223 were up-regulated and 292 were down-regulated. GO enrichment analysis showed that up-regulated DEGs were mainly involved in negative regulation of cell cycle, transcriptional control. KEGG signaling pathways analysis showed that up-regulated DEGs were mainly enriched in cell cycle signaling pathways. A total of 33 hub genes were screened through the PPI. UCLCAN analysis was implemented and 7 of 33 genes were relative to lower survival rate of CC patients. The expression levels of 7 genes by GEPIA analysis (P＜0.05).It was verified by GEPIA database that CCNB1, CCNA2, CDC20, CDKN3, DLGAP5, HMMR and NCAPG were highly expressed in colon cancer tissues. KEGG pathway enrichment and found that three critical genes (CCNB1, CDC20 and CCNA2) enriched in cell cycle pathway. The inhibition of CCNB1, CDC20 or CCNA2 significantly promoted proliferation of colon cancer cells. Conclusions A total of 7 key genes were identified to be involved in the occurrence of CC. The expression of CCNB1, CDC20 and CCNA2 is potentially related to the poor prognosis in CC, which may be potential targets of clinical treatment and prognostic markers for CC patients. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effect of silent information regulator 2 （SIRT2） overexpression on the differentiation of CD4+T cells into Th17 cells in the colon cancer microenvironment and its influence on hypoxia-inducible factor-1α （HIF-1α）. Methods: CT26 overexpressed SIRT2 in mouse colon cancer cells, and a stable SIRT2 overexpressed CT26 cell line was constructed （CT26/SIRT2）. The levels of SIRT2 and HIF-1α were detected by qRT-PCR and Western blot; and the effect of SIRT2 overexpression on the proliferation ability of CT26 cells was verified by CCK-8 method. Twenty-four healthy C57BL/6 mice were randomly separated into CT26 group and CT26/SIRT2 group, inoculated with CT26 cells and CT26/SIRT2 cells, respectively. Mice were sacrificed after 28 days, the proliferation and apoptosis of mouse tumor tissue cells were observed by Ki67 staining and TUNEL staining, and the levels of IL-17 and IL-6 in the supernatant of tissue homogenate were determined; Th17 cells were isolated by flow cytometry, and the levels of SIRT2 and HIF-1α in Th17 cells were detected by qRT-PCR and Western blot. Results: Compared with CT26 cells, CT26/SIRT2 cells had higher SIRT2 mRNA and protein levels, and lower HIF-1α mRNA and protein levels（ P<0.05）; there was no significant difference in the proliferation inhibition rates of CT26 and CT26/SIRT2 cells （P>0.05）; compared with CT26 mice, CT26/SIRT2 mice had decreased tumor volume and weight, positive expression of Ki67, proportion of Th17 cells in mouse tumor tissues, levels of IL-17 and IL-6 in tissue homogenate supernatant, mRNA and protein levels of HIF-1α in Th17 cells（ P<0.05）; and increased apoptotic rate of tumor cells, the levels of SIRT2 mRNA and protein in Th17 cells （P<0.05）. Conclusion: SIRT2 can inhibit the differentiation of CD4+ T cells into Th17 cells in the colon cancer microenvironment and down-regulate the expression of HIF-1α. [ABSTRACT FROM AUTHOR]

Copyright of Food Research & Development is the property of Food Research & Development Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To investigate the role of macrophage migration inhibition factor （MIF） in colon cancer and its possible regulatory mechanism. Methods: MIF expression in colon cancer tissues and para-carcinoma tissues was evaluated by qRT-PCR; expression of MIF in colon cancer cell lines HCT116 and a normal cell line HIEC-6 were detected by qRT-PCR and immunofluorescence. MIF expression was knocked down in vitro using si-RNA. Cell proliferative and migratory capacities were assessed by CCK-8, Transwell and scratch test, respectively. Long non-coding RNA, Zinc finger E-box binding homeobox 1 antisense 1 （lncRNA-ZEB1-AS1） expression was analyzed via qRT-PCR analysis. The interaction between lncRNA-ZEB1-AS1 and miR-200b were predicted by starBase software, and then verified by dual-luciferase reporter assay. Detection of HCT116 proliferation changes after overexpression of lncRNA-ZEB1-AS1 and silencing miR-200b. Results: MIF was significantly upregulated in colon cancer tissues. MIF has high expression in HCT116 cells while low expression in HIEC-6 cells. Furthermore, in vitro assays of silencing MIF inhibited HCT116 cell proliferation and migration ability, and MIF level were diminished in accordance with the MIF knockdown. starBase and dual-luciferase reporter assays suggested that lncRNA-ZEB1-AS1 inhibits the transcriptional activity of miR-200b promoter. Effects of decreased proliferation ability of colon cancer cells with knockdown of MIF could be significantly reversed by miR-200b silencing or lncRNAZEB1-AS1 overexpression. Conclusion: MIF may promote the proliferation and metastasis of colon cancer cells by activating the ZEB1-AS1/miR-200b signaling pathway. [ABSTRACT FROM AUTHOR]