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Purpose: To explore the effects of a self-designed Kirschner wire guiding and adjustment apparatus for internal fixation with cannulated screws for the treatment of femoral neck fracture. Methods: We retrospectively reviewed the patients with femoral neck fracture (Garden I-III) treated at our hospital between 01/2018 and 3/2022. The cases were included in the present study according to the inclusion and exclusion criteria. The operation time, The times of provisional Kirschner wires(K-wires) insertion, times of fluoroscopy , estimated blood loss in operation, Harris score, and VAS score of the hip joint were recorded and analyzed. Results: Forty patients were included (13 females and 17 males, (median, 58 years of age), with 20 patients in the unguided and 20 in the guided groups, respectively. Their body mass index (BMI) was 23.03±1.86 kg/m2. Compared with the unguided group, the guided group showed shorter operation time (median 0.20 vs. 0.43 h, PConclusions: Using theself-designed Kirschner wire guiding and adjustment apparatus during fixation of femoral neck fracture with cannulated screws reduces the operation time, blood loss, insertion times of Kirschner wire and fluoroscopy. This might promote the recovery of patients. Those results should be confirmed in further studies. Levels of Evidence: Level IV

Purpose Degenerative joint disease (DJD) of the ankle is a chronic disease that can severely limit function and cause debilitating pain, and with the development of digital medicine, 3D printing patient-specific instrumentation has been used in many subjects. The purpose of the study was to compare the clinical and radiographic outcomes of 3D-printed patient-specific guides with the traditional open- wedge supramalleolar osteotomy . Materials and methods We retrospectively analyzed 10 patients with varus ankle osteoarthritis treated by open wedge supramalleolar osteotomy via 3D patient-specific instrument (PSI group) and 14 patients treated via the traditional method (control group). The demographic data and the pre- and post-operative TAS, TT, TLS angle were recorded. The AOFAS and VAS score were acquired pre-operatively and at the last follow-up time. Results All patients were obtained after surgery 49.4 ± 8.3 months (36–62) follow-up. The TAS, TT, TLS angle and VAS, AOFAS score was comparable pre-operatively between two groups(p＞0.05). The VAS and AOFAS score was statistically improved at the last follow-up time in both cohorts. And the TAS angle was significantly increased post-operatively in the overall cohort. The TT,TLS angle was also ameliorated, though insignificantly. The intraoperative fluoroscopy time, estimated blood loss, and operating time was statistically less in the PSI group in the two cohorts. The post-operative TAS, TT, TLS angle and VAS, AOFAS score at the last follow-up time was comparable between the two cohorts. Conclusion 3D-printed patient-specific guides have a short operation time, low intraoperative blood loss and less fluoroscopy frequency. Patient-specific guides can assist in facilitating doctor-patient communication, shortening the learning curve, reducing surgery time, and correcting varus deformity accurately. And the functional outcome was non-inferior to the traditional method.

Based on high order polynomial approximation and dimension reduction technique, we propose a novel numerical method for the fourth order Steklov problems in the circular domain. We first decompose the primal problem into a set of 1D problems via polar coordinate transformation and Fourier basis functions expansion. Then, by introducing a non-uniformly weighed Sobolev space, the variational form and corresponding discrete scheme are derived. Employing the Lax-Milgram lemma and approximation properties of the projection operators, we further prove existence and uniqueness of weak solutions and approximation solutions for each one-dimensional problems, and the error estimation between them, respectively. We also carry out ample numerical experiments which illustrate that the numerical algorithm is efficient and highly accurate.

Introduction: The current molecular classification of small cell lung cancer (SCLC) based on expression of four lineage transcription factors, SCLC-A (ASCL1), SCLC-N (NEUROD1), SCLC-P (POU2F3), and SCLC-Y (YAP1) still leaves its major subtype SCLC-A as a large heterogeneous group, necessitating more precise characterization of lineage subclasses. Experimental procedure: To refine the current SCLC classification and to identify specific lineage features of the SCLC subtypes, we performed unsupervised hierarchical clustering of H3K27ac profiles on transcriptional regulators from 25 SCLC cell lines and determined the epigenomic features for each cluster. Functional significance of the transcriptional lineage regulators for the identified cluster was evaluated by cell growth, apoptosis and xenograft using CRISPR-Cas9-mediated deletion. The specific cistromic profiles by ChIP-seq and its functional transcriptional partners using co-immunoprecipitation followed by mass spectrometry were determined to reveal their functional output in the identified subtype. Rb1fl/flTrp53fl/fl and Rb1fl/flTrp53fl/flNkx2-1fl/fl genetic engineered mouse model were generated to explore the function of Nkx2-1 in tumor initiation and differentiation. H3K27ac profiles were further analyzed to reveal 6 human SCLC specimen and 20 mice tumors epigenomic landscapes. Summary: We identified previously uncharacterized epigenomic sub-clusters of the major SCLC-A subtype, named SCLC-A1 and SCLC-A2. SCLC-A1 was characterized by the presence of a super-enhancer at the NKX2-1 locus, which was observed in human SCLC specimens and a murine SCLC model. We found NKX2-1, a dual lung and neural lineage factor, is uniquely relevant in SCLC-A1, where it maintains neural lineage rather than pulmonary epithelial identity. We further found maintenance of this neural identity in SCLC-A1 is mediated by collaborative transcriptional activity with another neuronal transcriptional factor SOX1. ? Conclusions: We comprehensively describe an additional epigenomic heterogeneity of the major SCLC-A subtype, and define SCLC-A1 subtype by the core regulatory circuitry representing NKX2-1 and SOX1 super-enhancers and their functional collaborations to maintain a neuronal linage state. Citation Format: ranran kong, Ayushi S. Patel, Takashi Sato, Seungyeul Yoo, Abhilasha Sinha, Yang Tian, Feng Jiang, Charles A. Powell, Eric Snyder, Jiantao Jiang, Shaomin Li, Hideo Watanabe. Transcriptional circuitry of NKX2-1 and SOX1 defines a previously unrecognized lineage subtype of small cell lung cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5709.

p38 mitogen-activated protein kinase (MAPK) signaling has been implicated in the cancer development and progression. However, the precise mechanism of this association remains unknown. The aim of the present study was to evaluate the association between p38 and cancer progression, including investigations into the effects on cell proliferation, resistance to thalidomide, indoleamine 2,3-dioxygenase (IDO) expression and prognosis in patients with esophageal cancer. The present retrospective study included patients with stage I-III esophageal cancer. A total of 228 patients with esophageal cancer were recruited to analyze the expression of phosphorylated (p)-p38 and IDO in tumor, and normal tissues through immunohistochemistry. Depression status was measured using the Zung Self-Rating Depression Scale. P38 cDNA was transfected into esophageal cancer cells to assess tumor cell viability, sensitivity to thalidomide treatment and IDO gene expression. Western blotting and flow cytometry was used to analyze protein expression alterations, and apoptosis in esophageal cancer cells. P-p38 protein was expressed in 68.9% of cancer tissues, and was significantly associated with depressive symptoms, tumor recurrence and poor survival of patients. In vitro experiments revealed that the expression of p-p38 induced esophageal cancer Eca-109 and TE-1 cell viability, and resistance to thalidomide treatment, as well as in the expression of IDO without the application of lipopolysaccharides. Further follow-up of patients revealed that depression was also an independent factor for early recurrence and overall survival rate. Altered p38 MAPK expression was associated with poor outcome in patients with esophageal cancer. p38 may be a potential biomarker for the prediction of depressive symptoms and prognosis in patients with esophageal cancer.

DEAD (Asp-Glu-Ala-Asp) box protein 5 (DDX5), a prototypical member of the DEAD/H-box protein family, has been involved in several human malignancies. However, the expression and biological role of DDX5 in esophageal cancer (EC) remain largely unknown. In this study, we examined the role of DDX5 in regulating EC cell proliferation and tumorigenesis and explored its possible molecular mechanism. We found that DDX5 was overexpressed in human EC cell lines. In addition, knockdown of DDX5 significantly inhibited the proliferation of EC cells in vitro and the growth of EC xenografts in vivo. Knockdown of DDX5 also suppressed the migration/invasion and epithelial-to-mesenchymal transition (EMT) phenotype in EC cells. Furthermore, we observed that knockdown of DDX5 inhibited the expression of β-catenin, c-Myc, and cyclin D1 in EC cells. In conclusion, our findings provide the first evidence that siRNA-DDX5 inhibited the proliferation and invasion of EC cells through suppressing the Wnt/β-catenin signaling pathway. Therefore, DDX5 may be a novel potential therapeutic target for the prevention and treatment of EC.

Circular RNAs (circRNAs) have good stability and long half-life in blood and other body fluid, and possess regulatory effects on various biological processes as miRNA/RNA-binding protein sponges, or by competing endogenous RNA, indicating their great potential as biomarkers or targets of cancer therapy. In this study, we mainly explored the role and mechanism of circular RNA SMARCA5 (circsSMARCA5) in non-small cell lung cancer (NSCLC). Quantitative RT-PCR was applied to measure the expression levels of genes, and then, the relationships among circsSMARCA5, microRNA-670-5p (miR-670-5p), and RBM24 were further analyzed. Animal and cell experiments were performed to explore the functions of circsSMARCA5 in NSCLC cells. The results showed that circsSMARCA5 was expressed at low level in NSCLC tissues and cells, while miR-670-5p had high level in NSCLC tissues. Dual luciferase reporter assay verified that miR-670-5p was the target of circsSMARCA5, and RBM24 has the binding site of miR-670-5p. Further analysis showed that circsSMARCA5 could negatively regulate miR-670-5p and had positive relationship with RBM24. Moreover, circsSMARCA5 obviously inhibited tumor growth in vivo, reduced cell proliferation and increased cell apoptosis in vitro, while miR-670-5p mimic or RBM24 knockdown could reverse these effects. Thus, circsSMARCA5 may serve as an NSCLC suppressor by regulating the miR-670-5p/RBM24 axis, and it may have the potential to be a biomarker or therapeutic target for NSCLC.

The ribosomal protein (RP)‐p53 pathway has been shown to play a key role in apoptosis and senescence of cancer cells. miR-1908 is a newly found miRNA that was reported to have prognostic potential in melanoma. However, its role and mechanism in the progression of non-small cell lung cancer (NSCLC) are largely unknown. In this study, we found that expression of miR-1908 was significantly downregulated in human NSCLC cell lines, including SK-MES-1, A549, and NCI-H460. Then the role of miR-1908 in NSCLC cell proliferation was explored. The miR-1908 mimic was transfected into NSCLC cell lines, and their proliferation was detected. MTT and Cell Titer-Blue H analyses showed that the cell proliferation was notably reduced by the miR-1908 mimic transfection. Moreover, we found the RP‐p53 pathway was activated by miR-1908 mimic. Moreover, the miR-1908 inhibitor transfection had a completely opposite effect on the NSCLC cell proliferation than that of miR-1908 mimic. To explore the underlying mechanism of that, TargetScan bioinformatics server and 3′-UTR luciferase reporter assay were applied to identify the targets of miR-1908. Our results showed that AKT1 substrate 1 (AKT1S1), a newly proven suppressor of the RP‐p53 pathway, was a target of miR-1908, suggesting a probable mechanism for miR-191 suppressing NSCLC cell proliferation. Our findings provide a novel molecular target for the regulation of NSCLC cell proliferation.

Xingcong Ma,1 Wanjun Yan,1 Zhijun Dai,1 Xiaoyan Gao,1 Yinan Ma,1 Quntao Xu,2 Jiantao Jiang,3 Shuqun Zhang11Department of Oncology, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, People's Republic of China, 2Department of Oncology, Institute of Health, China North Industries Group Corporation, Xi'an, Shaanxi, People's Republic of China,3Department of Thoracic Surgery, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, People's Republic ofChinaBackground: The flavonoid baicalein, a historically used Chinese herbal medicine, shows a wide range of biological and pharmaceutical effects, among which its potent antitumor activity has raised great interest in recent years. However, the molecular mechanism involved in the antimetastatic effect of baicalein remains poorly understood. This study aimed to verify the inhibitory effects of baicalein on metastasis of MDA-MB-231 human breast cancer cells both in vitro and in vivo, as well as to investigate the related mechanisms.Methods: MTT assay was used to examine the inhibition of baicalein on proliferation of MDA-MB-231 cells. Wound healing assay and the in vitro invasion assay was carried out to investigate the effects of baicalein on migration and invasion of MDA-MB-231 cells, respectively. In order to explore the effects of baicalein on tumor metastasis in vivo, xenograft nude mouse model of MDA-MB-231 cells was established. Animals were randomly divided into four groups (control, therapy group, and low-dose and high-dose prevention group, n=6), and treated with baicalein as designed. Following sacrifice, their lungs and livers were collected to examine the presence of metastases. qRT-PCR and Western blot were performed to study the effects of baicalein on expression of SATB1, EMT-related molecules, and Wnt/β-catenin signaling components of MDA-MB-231 cells as well as the metastatic tissue. Effects of baicalein on the expression of target proteins in vivo were also analyzed by immunohistochemistry.Results: Our results indicated that baicalein suppressed proliferation, migration, and invasion of MDA-MB-231 cells in a time- and dose-dependent manner. Based on assays carried out in xenograft nude mouse model, we found that baicalein inhibited tumor metastasis in vivo. Furthermore, baicalein significantly decreased the expression of SATB1 in MDA-MB-231 cells. It suppressed the expression of vimentin and SNAIL while enhancing the expression of E-cadherin. Baicalein also downregulated the expression of Wnt1 and β-catenin proteins and transcription level of Wnt/β-catenin-targeted genes.Conclusion: Our results demonstrate that baicalein has the potential to suppress breast cancer metastasis, possibly by inhibition of EMT, which may be attributed to downregulation of both SATB1 and the Wnt/β-catenin pathway. Taken together, baicalein may serve as a promising drug for metastasis treatment of breast cancer.Keywords: breast cancer, baicalein, metastasis, EMT, SATB1, Wnt/β-catenin pathway

The incidence of non-small cell lung cancer (NSCLC) has significantly increased in China, while the prognosis of affected patients is poor. The pathogenesis of NSCLC is thought to be regulated by microRNAs (miRs). The present study used a miR array in order to determine the expression of miR-361-5p, which was significantly lower in NSCLC tissues compared with that in adjacent tissues, indicating a crucial role of miR-361-5p during the progression of NSCLC. Furthermore, the effects of transfection-induced upregulation of miR-361-5p on the NSCLC cell line H23 were assessed. Overexpression of miR-361-5p inhibited the proliferation and colony formation ability of H23 cells. In addition, apoptosis of H23 cells was induced by upregulation of miR-361-5p. Furthermore, signal transducer and activator of transcription 6 (STAT6) was confirmed as a direct target of miR-361-5p by a dual-luciferase reporter assay. Moreover, inhibition of STAT6 by small interfering RNA or miR-361-5p also decreased the expression of B-cell lymphoma extra large (Bcl-xL). In vivo, miR-361-5p significantly reduced tumor growth in a nude mouse xenograft model, and suppressed STAT6 and Bcl-xL expression. In conclusion, the present study indicated that miR-361-5p may represent a novel molecular tool for therapeutic and diagnostic strategies in NSCLC.

Objective: To evaluate the diagnostic value of endoscopic ultrasonography (EUS) in preoperative staging of esophageal carcinoma (EC).Material and methods: A total of 86 surgical patients with EC who were confirmed by endoscopy and biopsy underwent preoperative TN staging with EUS examination. The EUS findings were compared with surgical pathologic results.Results: The accuracy of EUS in T and N staging of EC was 82.6% and 84.9%, respectively. While determining whether EC invades the muscularis propria or outer membrane, EUS had the favorable sensitivity, specificity, positive predictive value and negative predictive value. The short-axis diameter of lymph nodes of 5mm had high sensitivity and negative predictive value to determine malignance with low specificity and positive predictive value. The short-axis diameter of 10mm presented the satisfactory sensitivity, specificity, positive predictive value and negative predictive value.Conclusion: EUS can accurately determine the TN staging of EC and p...

MicroRNAs (miRNAs) play critical roles in the development and progression of various cancers, including non-small-cell lung cancer (NSCLC). Studies have suggested that miR-330-5p is involved in the progression of several cancers. However, the role of miR-330-5p in NSCLC remains unclear. We investigated the effect on and mechanism of miR-330-5p in the progression of NSCLC. We found that miR-330-5p was significantly downregulated in NSCLC tissues and cell lines as detected by real-time quantitative polymerase chain reaction (RT-qPCR). The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), bromodeoxyuridine (BrdU), colony formation and cell cycle assays showed that overexpression of miR-330-5p markedly inhibited cell growth. Annexin V-FITC/PI and caspase-3 activity assays showed that overexpression of miR-330-5p significantly promoted cell apoptosis of NSCLC cells. Bioinformatics analysis and dual-luciferase reporter assays confirmed NIN/RPN12 binding protein 1 (NOB1) as a target gene of miR-330-5p. RT-qPCR and Western blot analysis showed that overexpression of miR-330-5p inhibited the expression of NOB1 as well as cyclin D1 and cyclin-dependent kinase 4 in NSCLC cells. Moreover, overexpression of NOB1 markedly reversed the miR‑330-5p-mediated inhibitory effect on NSCLC cell growth. Correlation analysis showed that miR‑330-5p expression was inversely correlated with NOB1 mRNA expression in NSCLC tissues. Taken together, our results indicate that miR-330-5p inhibits NSCLC cell growth through downregulation of NOB1 expression. Our study suggests that miR-330-5p may serve as a potential therapeutic target for the treatment of NSCLC.

The aim of the present study was to investigate the inhibitory effects of dihydroartemisinin (DHA) on the primary tumor growth and metastasis of the human breast cancer cell line, MDA-MB-231, in vitro. The expression levels of urokinase-type plasminogen activator (uPA) were detected by immunocytochemistry in two cell lines (MCF-7 and MDA-MB-231). The MDA-MB-231 cell activity was inhibited by various concentration gradients of DHA. The inhibitory rate, cell growth curve and apoptotic morphological observations were obtained using the MTT assay at 0, 24, 48 and 72 h. Cell scratch migration was performed at various time-points to test the cell proliferation and migration capacity. Reverse transcription-polymerase chain reaction was used to analyze the effect of DHA on uPA mRNA expression in breast cancer cells. The human breast cancer cell line, MDA-MB-231, possesses higher metastatic potential and relatively higher expression of uPA when compared with the MCF-7 cell line. DHA was found to inhibit the proliferation and migration capacity of the cell line, MDA-MB-231, in vitro. The growth inhibition occurred in a time- and dose-dependent manner, with IC50 values of 117.76±0.04, 60.26±0.12 and 52.96±0.07 μmol/l following 24, 48 and 72 h, respectively. The inhibition of uPA was observed to decrease breast cancer cell growth and migration. Thus, results of the present study indicate that DHA may be used for further studies with regard to breast cancer therapy.

An efficient palladium-catalysed protocol for direct C–H bond acylation by cross coupling of 2-arylbenzo[d]thiazoles and aldehydes using tert-butyl hydroperoxide as the oxidant is reported. The process provides a useful method for the synthesis of aromatic ketones directly from aldehydes. In addition, the reaction can tolerate various functional groups in good yield with high regioselectivity.

Background miR-126 is a key regulator of oncogenic processes. It is functionally linked to cellular proliferation, survival and migration. Vascular endothelial growth factor A (VEGF-A), which is regarded as a tumorgenesis activator, could directly target miR-126 in several tumors. However, the mechanism in esophageal cancer remains unclear. Methods and results In this study, the expression of miR-126 and VEGF-A were assessed in esophageal cancer tissues and esophageal cancer cell lines. We found that miR-126 has significantly lower expression in esophageal cancer tissues and esophageal cancer cell lines than in healthy tissues, while the expression of VEGF-A is high. Luciferase reporter assays were performed to investigate the relationship between VEGF-A and miR-126. We confirmed that VEGF-A is a target for miR-126. Furthermore, the proliferation of esophageal cancer cells with miR-126 overexpression and miR-126 knockdown was monitored using the MTT assay. The results showed that miR-126 could inhibit esophageal cancer cell proliferation in vitro. The effect of miR-126 was also detected in BALB/c nude mice with transplanted esophageal cancer cells. In vivo study showed that tumor growth was significantly suppressed by miR-126 overexpression. Conclusions We believe that restoring miR-126 levels may be a promising therapeutic approach in cases of esophageal cancer.

Lung cancer is the leading cause of cancer-related deaths worldwide. Squamous cell carcinoma is one of the predominant histological subtypes of lung cancer. Detecting lung cancer at an early stage is essential for successful therapy and increasing survival. There are still no satisfactory biomarkers for the early detection of lung cancer. In this study, tumour tissue paired with tumour-adjacent normal bronchial epithelial tissue was obtained from patients with squamous cell lung carcinoma without metastasis. The proteins extracted from the cell membrane were separated by two-dimensional polyacrylamide gel electrophoresis (2-DE) and were analysed with the Image Master two-dimensional platinum software. Twenty-five significantly different protein spots were selected and identified with matrix-assisted laser desorption/ionisation time-of-flight mass spectrometry (MALDI-TOF MS). A total of 19 proteins were successfully identified. Twelve proteins were up-regulated, and seven proteins were down-regulated in the cancerous tissue compared with the tumour-adjacent normal tissue. One up-regulated protein and one down-regulated protein in squamous cell lung carcinoma were verified by Western blot analysis and RT-PCR; the results were consistent with the 2-DE analysis. In conclusion, membrane proteomics identified a number of candidate biomarker proteins that were differentially expressed between squamous cell lung cancer tissue and adjacent normal tissue. These biomarker candidates have the potential to elucidate the underlying pathogenesis of squamous cell lung cancer.

Non-small cell lung cancer (NSCLC) is the most common type of lung tumor with poor prognosis, in which the Notch signaling pathway plays an important role. Notch activation complex kinase (NACK) has been reported both as a co-activator and a target gene of the Notch pathway. However, the molecular mechanism of NACK in NSCLC still remains unknown. In this study, the expression of NACK was analyzed in 35 paired NSCLC tumor samples and 2 NSCLC cell lines. MTT assay, cell migration assay, cell invasion assay, flow cytometry assay, and xenograft model were employed to detect the effect of NACK knockdown on the cell proliferation, metastasis, invasion and apoptosis of NSCLC. The relationship between NACK and Notch1 signaling pathway in NSCLC cells was assessed by western blot and luciferase reporter assay. We found that the expression of NACK in the NSCLC tissues and lung cancer cells were significantly increased. High level of NACK expression is remarkable associated with tumor differentiation, lymphatic metastasis, clinical stage and poor survival prognosis. The interference of NACK significantly inhibited cell proliferation, invasion and metastasis through inducing apoptosis in NSCLC cells. The transcriptional activity of related Notch1 target genes were significantly suppressed resulting from NACK knockdown. This study demonstrates that interference of NACK inhibits NSCLC progression through Notch1 signaling pathway and targeting NACK may be an effective approach for NSCLC therapy.

Special AT-rich sequence binding protein 1 (SATB1) is a recently discovered gene regulator that can promote the growth and metastasis of breast cancer. However, its expression in different stages of breast cancer development have not been examined. We explored the role of SATB1 in the development of breast cancer by detecting SATB1 expression levels in different stages of breast cancer. SATB1 expression was determined using an immunohistochemical streptavidin peroxidase method; the relationship between clinicopathological features of breast cancer and SATB1 expression was analyzed using the X(2) test. Positive rates of SATB1 protein in normal breast tissue, normal breast ductal hyperplasia tissue, precancerous lesions of breast cancer, non-invasive cancer, early invasive carcinoma, and invasive breast cancer tissue were, respectively, 6.25 (2/32), 6.4 (3/47), 20.4 (10/49), 45.0 (9/20), 52.9 (9/17), and 76.6% (72/94). SATB1 in the latter 3 groups was significantly higher than in the first 3 groups (P < 0.05). The positive rate of SATB1 protein in invasive non-special types of breast cancer (88.5%, 54/61) was significantly higher than in the special type of invasive breast cancer (54.5%, 18/33) and early invasive breast cancer (52.9%, 9/17) (P < 0.05). SATB1 protein expression in breast cancer with lymph node metastasis was generally increased, and the difference was statistically significant (P < 0.05). SATB1 protein expression showed an increasing trend in different stages of breast cancer development. Overexpression indicated poor prognosis.

O-linked N-acetylglucosamine transferase (OGT) catalyzes O-linked glycosylation (O-GlcNAcylation). O-GlcNAcylation is a post-translational carbohydrate modification of diverse nuclear and cytosolic proteins by the addition of O-linked β-N-acetylglucosamine. It was recently demonstrated that OGT and the level of O-GlcNAcylation are upregulated in esophageal cancer; however, the physiological consequences of this upregulation remain unknown. The current study reports that OGT knockdown by short hairpin RNA (shRNA) did not affect cell viability; however, cell migration in esophageal cancer Eca-109 cells was significantly reduced. OGT-specific shRNA vectors efficiently decreased the protein and mRNA levels of OGT and the RL2 level (a marker of O-GlcNAcylation levels) in Eca-109 esophageal cancer cells. In addition, colony formation and cell proliferation assays demonstrated that OGT-specific shRNA decreased the proliferation of Eca-109 cells; however, there was no significant statistical difference between OGT-specific shRNA and control shRNA. Notably, transwell assays demonstrated that the migratory ability of Eca-109 cells was significantly suppressed following knockdown of the OGT gene. Correspondingly, western blot analyses demonstrated that OGT knockdown significantly downregulated the expression of matrix metalloproteinase 9 (MMP9) in Eca-109 cells. These results suggest that OGT may promote the migration, invasion and metastasis of esophageal cancer cells by enhancing the stability or expression of MMP9.

AIM To evaluate PIK3CA gene mutational status in Northwest Chinese esophageal squamous cell carcinoma (ESCC) patients, and examine the associations of PIK3CA gene mutations with clinicopathological characteristics and clinical outcome. METHODS A total of 210 patients with ESCC who underwent curative resection were enrolled in this study. Pyrosequencing was applied to investigate mutations in exons 9 and 20 of PIK3CA gene in 210 Northwest Chinese ESCCs. The associations of PIK3CA gene mutations with clinicopathological characteristics and clinical outcome were examined. RESULTS PIK3CA gene mutations in exon 9 were detected in 48 cases (22.9%) of a non-biased database of 210 curatively resected Northwest Chinese ESCCs. PIK3CA gene mutations were not associated with sex, tobacco use, alcohol use, tumor location, stage, or local recurrence. When compared with wild-type PIK3CA gene cases, patients with PIK3CA gene mutations in exons 9 experienced significantly better disease-free survival and overall survival rates. CONCLUSION The results of this study suggest that PIK3CA gene mutations could act as a prognostic biomarker in Northwest Chinese ESCC patients.

This strategy can be used for the direct synthesis of aromatic ketones from aldehydes and is compatible with a variety of functional groups including electron-donating and -withdrawing groups attached to both 2-arylbenzo[d]thiazoles and aldehydes.

Objective: To investigate uPA and VEGF expression in esophageal cancer and relations with tumorous invasion and metastasis. Methods: Immunohistochemistry was used to detect uPA and VEGF expression in the normal epithelial tissue of esophageal mucosa and cancer tissue and detect CD34 labeled micrangium and analyze the relationships with clinical pathological features and tumor angiogenesis. Results: Positive rates for uPA and VEGF protein expression were significantly greater in esophageal cancer than normal epithelial tissue ( P < 0.05), the two being linked (P

The aim of this present study was to explore the expression and clinical significance of O-linked N-acetylglucosamine (O-GlcNAc) transferase (OGT) and enzymatic O-linked glycosylation (O-GlcNAcation) through the addition of O-linked-β-N-acetylglucosamine in esophageal squamous cell carcinoma. OGT expression and O-GlcNAcation in 40 samples from patients with esophageal squamous cell carcinoma was detected by immunohistochemical staining with anti-OGT antib ody and O-GlcNAc-specific antibody RL2, respectively. The relationship between pathological and clinical factors of patients was analyzed. We found that the expression of OGT was higher in esophageal squamous cell carcinoma samples compared to the normal tissues. RL2 antibody level was positively correlated with OGT expression, and the metastasis of lymph node, which means the level of O-GlcNAcation was high and related to the metastasis of lymph node in esophageal squamous cell carcinoma. In conclusion, OGT activation is the main reason for promoting the level of O-GlcNAcation in esophageal squamous cell carcinoma. O-GlcNAcylation may play an important role in esophageal squamous cell carcinoma.