Search

ObjectiveTo explore the role of MAPK4 in cervical squamous cell carcinoma (CSCC) for the identification of candidate prognostic prediction biomarkers and molecular therapeutic targets. MethodsThe TCGA cohort was subjected to Kaplan-Meier survival analysis. Immunohistochemistry experiments were conducted on clinical samples to explore the correlation between MAPK4 and patient prognosis. A nomogram was constructed based on MAPK4 mRNA levels. Western blot, CCK-8, colony formation, and Transwell cell function experiments were performed to clarify the abnormal expression and role of MAPK4 in CSCC. DIA proteome sequencing was used to identify effector molecules regulated by MAPK4. Combined with the above cell function experiments, the knockdown of MAPK4 and the overexpression of effector molecules revealed that MAPK4 regulated effector molecules to mediate tumor progression. ResultsCSCC patients with elevated MAPK4 mRNA levels and high protein expression have a worse prognosis. The constructed nomogram based on MAPK4 can accurately predict the 1-, 3-, and 5-year survival rates of patients. Compared with that in normal cervical tissues, MAPK4 protein expression was up-regulated in tumors. MAPK4 knockdown substantially inhibited the proliferation, colony formation, migration, and invasion of CSCC ME180 and SiHa cells. SLC3A2 is a downstream effector molecule of MAPK4. Overexpression SLC3A2 can weaken the inhibitory effect of MAPK4 knockdown on cell proliferation, colony formation, migration, and invasion. ConclusionMAPK4 is a candidate prognostic biomarker for patients with CSCC. MAPK4 positively regulates SLC3A2 protein expression and accelerates tumor progression, making it a potential molecular therapeutic target for patients with CSCC.

Objective To analyze the prognostic characteristics of different invasion sites and the risk factors affecting overall prognosis, in patients with pT4b stage colorectal cancer who underwent radical resection and showed no lymph node metastasis （N0） by pathology. Methods The clinical and pathological data of colorectal cancer patients received surgical resection in China National Petroleum Corporation Central Hospital from 2017-01-01 to 2021-12-21 were calculated and followed up to 2022-12-31. The time of operation, the time of local recurrence or distant metastasis and the time of death were recorded. Risk factor analysis was grouped based on whether there was disease progression during follow-up. Prognosis of different groups was compared and logistic binary regression was used to screen for meaningful risk factors. Results Survival analysis showed that the disease-free survival (DFS) of patients with tumor invasion of abdominal wall or omentum was (22.2±3.2) months, DFS of tumor invasion of stomach or intestine was (28.3±5.6) months, DFS of tumor invasion of uterus or adnexal was (35.7±2.6) months, and DFS of tumor invasion of the bladder or ureteral was (30.1±3.4) months, Log-rank P=0.001 among groups. Multivariate analysis showed that the right colon (OR=6.829, 95%CI:1.603-29.093, P=0.009), tumor invasion of abdominal wall, omentum (OR=6.198, 95%CI:1.231-31.210, P=0.027), tumor maximum diameter (OR=0.565, 95%CI:0.365-0.874, P=0.010) were independent factors affecting the progression of colorectal cancer. Conclusion Among colorectal cancer patients with pathological staging pT4bN0M0, patients with tumor invasion of the uterus and appendix have the best prognosis, while patients with invasion of the abdominal wall and omentum have the worst prognosis. Patients with tumors located in the right colon and invading the abdominal wall, omentum, or smaller tumor lesions are more likely to experience regional recurrence or distant metastasis after surgery.

Background Targeted therapy, represented by epidermal growth factor receptor-targeting tyrosine kinase inhibitors (EGFR-TKIs) , has significantly prolonged the survival time of patients with EGFR mutations with relatively mild adverse reactions, and become a prior choice for advanced non-small cell lung cancer (NSCLC) patients with driver genes. Dynamic monitoring of treatment progress and gene mutations in NSCLC patients by means of gene detection will help to provide a more effective, long-term and stable individualized targeted therapy for such patients. Objective To compare the gene mutations before and after the progression of NSCLC, and to analyze the regularities of gene mutations dynamically monitored and related prognostic value in NSCLC patients. Methods NSCLC outpatients and inpatients undergoing genetic tests were selected from Department of Integrated Medicine and Lung Cancer Center of China-Japan Friendship Hospital from 2007 to 2021. Their data were collected and used to establish a lung cancer genes testing database. Tissue samples or peripheral blood circulating tumor DNA (ctDNA) before and after progression were obtained for full-coding area detection of lung cancer genes, and the number of gene mutations and testing results were recorded. We divided enrolled patients into gene clearance group and non-gene clearance group, and compared baseline characteristics and survival status between the groups. Results A total of 217 cases were enrolled and followed until their clinical endpoint. The total changes in gene mutations in tissue samples before and after the disease progression were as follows: the number of patients with wild type increased from 70 (32.3%) to 95 (43.8%) , the number of patients with mutant type decreased from 147 (67.7%) to 122 (56.2%) , the number of patients with 19DEL mutation increased from 64 (29.5%) to 67 (19.8%) , the number of patients with 21 L858R mutations decreased from 74 (34.1%) to 64 (24.0%) , the number of patients with T790M mutations increased from 2 (0.9%) to 45 (20.7%) , and the number of those with rare mutations or concomitant rare mutations such as TP53 increased from 20 (9.2%) to 84 (38.7%) . Gene clearance group (n=67) and non-gene clearance group (n=150) had significant differences in clinical features except the history of lung disease (P=0.032) and the history of targeted therapy (P=0.001) . The median progression-free survival (PFS) of patients in the two groups was 9.8 months and 11.8 months, respectively, with no significant difference〔HR=0.89, 95%CI (0.66, 1.20) , P=0.310〕. The median PFS of 134 patients with advanced NSCLC in two groups was 8.1 months and 9.8 months, respectively, with no significant difference〔HR=0.83, 95%CI (0.58, 1.19) , P=0.359〕. The median overall survival (OS) of patients in two groups was 50.5 months and 28.5 months, respectively, with statistically significant difference〔HR=0.56, 95%CI (0.41, 0.78) , P

Diffuse large B-cell lymphoma (DLBCL) is a common, highly aggressive and heterogeneous hematologic malignancy in adults. Patients with DLBCL have substantially differences in molecular biological characteristics, clinical manifestations, and prognosis. Increasing evidence shows that the tumor microenvironment plays an important role in the occurrence and development of DLBCL. CD47, an integrin related protein, is overexpressed in DLBCL cells and plays a key role in immune escape of lymphoma. This work reviews the research progress of CD47 in DLBCL TME in terms of CD47-related signal pathway, CD47 role in DLBCL TME, and therapeutic strategies targeting CD47 in DLBCL TME.

Diffuse large B-cell lymphoma (DLBCL) is a common, highly aggressive and heterogeneous hematologic malignancy in adults. Patients with DLBCL have substantially differences in molecular biological characteristics, clinical manifestations, and prognosis. Increasing evidence shows that the tumor microenvironment plays an important role in the occurrence and development of DLBCL. CD47, an integrin related protein, is overexpressed in DLBCL cells and plays a key role in immune escape of lymphoma. This work reviews the research progress of CD47 in DLBCL TME in terms of CD47-related signal pathway, CD47 role in DLBCL TME, and therapeutic strategies targeting CD47 in DLBCL TME. [ABSTRACT FROM AUTHOR]

The occurence and development of tumors is a complicated process, which not only depends on the mutation or deletion of genes, but also is affected by epigenetic regulation. Accumulating evidences have shown that epigenetic modifications play fundamental roles in transcriptional regulation, heterochromatin formation, X chromosome inactivation, DNA damage response and tumor development. SET domain containing lysine methyltransferase 7 (SETD7) was initially identified as an important lysine methyltransferase, which methylated histone and non-histone proteins. These modifications play fundamental roles. Once this modification disorders, it can directly lead to cell abnormalities and cause many diseases. Studies have shown that SETD7 is related to the occurence and development of various tumors, but the methylation sites of SETD7 and its regulatory mechanism have not been fully elucidated. This article summarizes the research progress of the role of SETD7 on histone and non-histone methylation modification in tumors and the molecular mechanism, in order to provide new therapeutic targets for tumor pathogenesis and diagnosis.

Objective To screen and verify hub genes TPM1 and CALD1 that can affect the diagnosis and prognosis of bladder cancer (BLCA). Methods We obtained gene chip expression data of 414 and 188 cases of bladder cancer from TCGA and GEO, respectively. By constructing a weighted gene co-expression network analysis (WGCNA) and identifying differentially-expressed genes between tumor tissues and normal tissues, the pivotal genes that were highly associated with bladder cancer were obtained, and the STRING database was used to construct a protein interaction network to screen out prognostic-related pivotal genes. We took 29 cases of bladder cancer samples from People's Hospital of Zhengzhou as external verification results. Results A total of 915 and 464 differentially-expressed genes were screened from the TCGA database and GSE13507, respectively. Two modules with the strongest correlation were obtained through WGCNA: the blue module (Pearson cor=0.60, P=1E-44) and the cyan module (Pearson cor=0.52, P=7E-19), and 156 intersection genes were obtained. Through protein interaction network analysis, 10 pivotal genes were screened out. TPM1 and CALD1 genes had the greatest correlation with the survival of bladder cancer patients, which was verified by external experimental verification group. Conclusion TPM1 and CALD1 are closely related to the prognosis of bladder cancer patients. They are also pivotal genes to promote tumor progression.

Copyright of Journal of Guangxi Normal University - Natural Science Edition is the property of Gai Kan Bian Wei Hui 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.)

A large body of evidence has demonstrated that serum levels of secreted protein YKL-40 (CHI3L1) were elevated in a broad type of human advanced cancers, suggesting that serum levels of YKL-40 serve as a cancer biomarker for the malignancy. The current study is to investigate the effects of recombinant protein YKL-40 and YKL-40 over-expressed by tumor cells on tumor epithelial mesenchymal transition (EMT). Two cancer lines breast cancer cell line MDA-MB-231 that displays a fibroblastic phenotype and colon cancer cell line HCT-116 that does not exhibit the fibroblastic morphology were selected to enforce expression of ectopic YKL-40. After both cell lines were established to stably express YKL-40, the cell phenotype was observed. EMT markers vimentin and N-cadherin proteins were analyzed by Western Blot. The cell cultured media were collected to test YKL-40 levels. Control and HCT-116 cells expressing ectopic YKL-40 were used to test cell survival in the presence of serum free medium for 72 h via a live and dead kit. Concomitantly, recombinant protein YKL-40 was added to parental MDA-MB-231 cells to observe cell survival in the serum-free medium for 72h. MDA-MB-231 cells expressing YKL-40 were employed to examine cell invasion and cultured media were exploited to test MMP9 expression via WB and enzymatic activity via zymography. MDA-MB-231 cells expressing YKL-40 displayed a more mesenchymal phenotype than control cells; whereas HCT-116 cells expressing YKL-40 showed subtle induction of a fibroblastic phenotype. MDA-MB-231 cells expressing YKL-40, but not HCT-116 cells expressing YKL-40, revealed elevated expression of vimentin and N-cadherin. YKL-40 or YKL-40-expressing tumor cells induced tumor cell survival. YKL-40-expressing MDA-MB-231 cells increased invasion and the expression and enzymatic activity of MMP9. YKL-40 has the ability to increase tumor cell survival and enhance EMT, pointing to YKL-40 as a therapeutic target for cancer treatment. [ABSTRACT FROM AUTHOR]

Background and objective It has been known that the volume doubling time (VDT) of different lung nodule types is different. At present, there is still a lack of studies about the volume doubling time of lung cancer with different pathological types. The purpose of the study is to explore the factors influencing the progression of the early-stage adenocarcinoma, and provide some reference for the follow-up strategy of lung nodules by retrospective analysis of the image data of 143 early-stage adenocarcinoma. Methods 143 cases of the early adenocarcinoma were classified according to the 2015 World Health Organization Classification of Lung Tumors and the Eighth edition of the tumor-node-metastasis (TNM) classification of lung cancer. The volume doubling time was calculated with reference to the revised Schwartz formula. Results Among the 143 cases of the early adenocarcinoma, 50 cases (34.97%) were in progression. By multivarIate analysis, there were several factors associated with the progression of the early adenocarcinoma: the follow-up time, the dimension of nodule, the pathological type, the nodule type and the pathological stage. The VDT of lepidic predominant adenocarcinoma (LPA) is (594±272) d. The VDT of the invasive adenocarcinoma with lepidic part, but not predominant, is (520±285) d. The VDT of the invasive adenocarcinoma without lepidic part is (371±183) d. Conclusion About 35% of the early adenocarcinoma is in progress. Whether with the lepidic component is a positive factor to the speed of tumor progression.

Osteopontin (OPN) is a multifunctional, extracellular matrix-associated, secretory, glyco-protein. It can be used as an adhesion protein involved in tumor cell adhesion,migration; but also as a cytokine, promoting tumor angiogenesis, evading immune surveillance and inhibiting cellular apoptosis. CD44v glycoprotein, is one of the cell surface adhesion molecule that mediates cell-matrix and cell-cell interactions. Extensive research has suggested the important role of OPN in regulating signaling pathways that contribute to tumor progression and metastasis, and the serum level is associated with the prognosis of various malignancies. Therefore, clarifying OPN in the molecular mechanisms of tumor progression and its signaling pathway contributes to seeking a novel anti-cancer therapy.

Copyright of Chinese Journal of Lung Cancer is the property of Chinese Journal of Lung Cancer 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 Lung Cancer is the property of Chinese Journal of Lung Cancer 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.)

The occurence and development of tumors is a complicated process, which not only depends on the mutation or deletion of genes, but also is affected by epigenetic regulation. Accumulating evidences have shown that epigenetic modifications play fundamental roles in transcriptional regulation, heterochromatin formation, X chromosome inactivation, DNA damage response and tumor development. SET domain containing lysine methyltransferase 7 (SETD7) was initially identified as an important lysine methyltransferase, which methylated histone and non-histone proteins. These modifications play fundamental roles. Once this modification disorders, it can directly lead to cell abnormalities and cause many diseases. Studies have shown that SETD7 is related to the occurence and development of various tumors, but the methylation sites of SETD7 and its regulatory mechanism have not been fully elucidated. This article summarizes the research progress of the role of SETD7 on histone and non-histone methylation modification in tumors and the molecular mechanism, in order to provide new therapeutic targets for tumor pathogenesis and diagnosis.
.

Tumor associated macrophages (TAMs) are one of the most common types of stromal cells in solid tumors. They are closely related to the immunosuppressive status of tumor microenvironment and potentiate the malignant progress of tumors. Studies have shown that metabolism in tumor associated macrophages has been reprogrammed and involved in the regulation of their own polarization and corresponding functions and phenotypes. Metabolic reprogramming refers to the alteration of key enzymes activity, substrate and its associated metabolites' concentration in a certain metabolic pathway, which accounts for the disorder of original metabolic states. In this paper, we mainly concentrated on the lipid metabolic reprogramming of TAMs, including triglycerides, fatty acids and their derivatives, cholesterol, phospholipids, and their regulations on tumor progression. However, the metabolism of tumor and tumor microenvironment cells is highly heterogeneous. It is worthy of further exploration on the similarities and differences of lipid metabolism reprogramming between stromal cells and tumor cells, and the mechanism of how reprogramming modulates cell activity. It will be a new strategy for immunotherapy of tumor with metabolic intervention to accurately target the lipid metabolism reprogramming of TAMs, so as to promote the polarization of TAMs to M1 like macrophages, when synthetically considering the diverse types of tumors and different stages of development., (Copyright© by Editorial Board of Journal of Sichuan University (Medical Sciences).)

Objective: To explore the role of Long noncoding RNA UFC1 (lincRNA-UFC1) in modulating the metastasis and invasion of hepatocellular carcinoma (HCC) cells and the underlying mechanism., Methods: Human HCC cell line Huh7 was infected with the lentiviral vector carrying lincRNA-UFC1 to obtain a cell line with lincRNA-UFC1 overexpression. A short hairpin RNA (shRNA) targeting lincRNA-UFC1 was delivered in human HCC BEL-7402 cells via a lentiviral vector to obtain a cell line with lincRNA-UFC1 knockdown. Expression levels of lincRNA-UFC1 in the two HCC cell lines were detected using real-time PCR, and the changes in the cell invasion and migration in response to lincRNA-UFC1 overexpression or knockdown were analyzed using Transwell and wound-healing assays. The expressions of GSK-3β/β-catenin-related proteins in the cells were detected with Western blotting. XAV-939, a GSK-3β/β-catenin inhibitor, was used for assessing the impact of lincRNAUFC1 overexpression on the invasion and migration of the HCC cells through Transwell and wound-healing assays., Results: Overexpression of lincRNA-UFC1 significantly promoted the invasion and migration of Huh7 cells as compared with the control cells ( P < 0.001), while lincRNA-UFC1 knockdown obviously suppressed the invasion and migration of BEL-7402 cells ( P < 0.001). The results of Western blotting showed that the expressions of proteins associated with the cell invasion and migration, namely β-catenin and P-GSK-3β, were significantly upregulated in response to lincRNA-UFC1 overexpression, and were obviously lowered after lincRNA-UFC1 knockdown. Treatment of the cells with XAV-939 significantly reversed the effect of lincRNA-UFC1 overexpression on the cell invasion and migration ( P < 0.001)., Conclusions: lincRNA-UFC1 overexpresison promotes cell invasion and migration through the GSK-3β/β-catenin axis in HCC cells in vitro .

Background: It has been known that the volume doubling time (VDT) of different lung nodule types is different. At present, there is still a lack of studies about the volume doubling time of lung cancer with different pathological types. The purpose of the study is to explore the factors influencing the progression of the early-stage adenocarcinoma, and provide some reference for the follow-up strategy of lung nodules by retrospective analysis of the image data of 143 early-stage adenocarcinoma., Methods: 143 cases of the early adenocarcinoma were classified according to the 2015 World Health Organization Classification of Lung Tumors and the Eighth edition of the tumor-node-metastasis (TNM) classification of lung cancer. The volume doubling time was calculated with reference to the revised Schwartz formula., Results: Among the 143 cases of the early adenocarcinoma, 50 cases (34.97%) were in progression. By multivarIate analysis, there were several factors associated with the progression of the early adenocarcinoma: the follow-up time, the dimension of nodule, the pathological type, the nodule type and the pathological stage. The VDT of lepidic predominant adenocarcinoma (LPA) is (594±272) d. The VDT of the invasive adenocarcinoma with lepidic part, but not predominant, is (520±285) d. The VDT of the invasive adenocarcinoma without lepidic part is (371±183) d., Conclusions: About 35% of the early adenocarcinoma is in progress. Whether with the lepidic component is a positive factor to the speed of tumor progression.