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MicroRNAs can regulate the transcription of protein‐coding genes associated with the development and progression of cancer. In this study, we explored the potential diagnostic function of exosome miR‐3184‐5p in gastric cancer. This exosome was isolated from the blood samples of 150 patients with gastric cancer and 60 healthy participants. The mean particle size and concentration of serum exosome in the patients with gastric cancer were 104.6 nm (93.97–115.84) and 6.21e+009 particles/ml (5.15e+009–7.12e+009), respectively. miR‐3184‐5p expression was substantially downregulated in the patients with gastric cancer compared with that in the healthy participants. The gastric cancer cell line HGC‐27 was cultured and transfected with the mimic and an inhibitor to overexpress and inhibit miR‐3184‐5p expression. miR‐3184‐5p strongly suppressed cell proliferation, migration, and invasion but induced cell apoptosis. Luciferase reporter assay revealed that XBP1 was the target of miR‐3184‐5p. miR‐3184‐5p substantially downregulated the expression of CD44, cyclin D1, MMP2, p65, p‐AKT, and p‐STAT3 but upregulated that of GRP78, IRE1, p‐JNK, and CHOP. Moreover, miR‐3184‐5p cleaved caspase‐12 and inhibited BCL‐2 expression. These results suggested that the downregulation of miR‐3184‐5p in patients with gastric cancer might regulate the AKT, STAT3, and IRE1 pathways to promote the vitality of gastric cancer cells. [ABSTRACT FROM AUTHOR]

Chemoresistance remains a major problem in the treatment of gastric cancer patients, leading to the serious limitation of efficacy of chemotherapeutic regime. However, the underlying mechanism remains largely unknown. In our present study, we for the first time found that knock down of KDM3A can promote apoptosis induced by chemoreagent Cisplatin and Paclitaxel through p53. Mechanistically, through promoting p53 binding to the promoter of PUMA. However, knock down of KDM3A as such doesn't affect p53 level. In addition, KDM3A can interact with p53K372me1 in protein–protein interaction fashion, leading to the inactivation of p53, may eventually leading to chemoresistance of gastric cancer. [ABSTRACT FROM AUTHOR]

Background: Endoscopic obstruction (eOB) is associated with a poor prognosis in colorectal cancer (CRC). Our study aimed to investigate the association between tumor location and eOB, as well as the prognostic differences among non-endoscopic obstruction (N-eOB), eOB with tumor size ≤ 5 cm, and eOB with tumor size > 5 cm in non-elderly patients., Methods: We retrospectively reviewed the clinicopathological variables of 230 patients with CRC who underwent curative surgery. The multivariable logistic regression model was used to identify risk factors for eOB. The association between eOB with tumor size ≤ 5 cm and disease-free survival (DFS) was evaluated using multivariate cox regression analysis., Results: A total of 87 patients had eOB while 143 had N-eOB. In multivariate analysis, preoperative carcinoembryonic antigen ( p = 0.014), tumor size ( p = 0.010), tumor location (left-side colon; p = 0.033; rectum; p < 0.001), and pT stage (T3, p = 0.009; T4, p < 0.001) were significant factors of eOB. The DFS rate for eOB with tumor size ≤ 5 cm was significantly lower ( p < 0.001) in survival analysis. The eOB with tumor size ≤ 5 cm ( p = 0.012) was an unfavorable independent factor for DFS., Conclusions: The patients with eOB were significantly associated with right-side colon cancer as opposed to left-side colon cancer and rectal cancer. The eOB with tumor size ≤ 5 cm was an independent poor prognostic factor. Further studies are needed to target these high-risk groups., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Yu, Lin, Wang, Hu, Xie, Que, Lai and Xu.)

Purpose: The aim to assess treatment failure in patients with stage III colon cancer who underwent radical surgery and was analyzed using the nomogram., Methods: Clinical factors and survival outcomes for stage III colon cancer patients registered in the SEER database from 2018 to 2019 were analyzed, with patients split into training and testing cohorts (7:3 ratio). A total of 360 patients from the First Affiliated Hospital of Longyan served as an external validation cohort. Independent predictors of treatment failure were identified using logistic regression analyses. The nomograms was evaluated by concordance index (C-index), calibration curves, and the area under the curve (AUC), decision curve analysis (DCA) and clinical impact curves (CIC) assessed the clinical utility of nomograms versus TNM staging., Results: The study included 4,115 patients with stage III colon cancer. Multivariate logistic analysis age, tumor site, pT stage, pN stage, chemotherapy, pretreatment CEA levels, number of harvested lymph nodes, perineural invasion and marital status were identified as independent risk factors for treatment failure. The C-indices for the training and testing sets were 0.853 and 0.841. Validation by ROC and calibration curves confirmed the stability and reliability of the model. DCA showed that the net clinical effect of the histogram was superior to that of the TNM staging system, while CIC highlighted the potentially large clinical impact of the model., Conclusions: The developed Nomogram provides a powerful and accurate tool for clinicians to assess the risk of treatment failure after radical surgery in patients with stage III colon cancer., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Zeng, Zhong, Liu, Liang, Xue, Yu, Xu, Wang and Lin.)

Objective: By in silico analysis of colon cancer data from the Cancer Genome Atlas (TCGA) database, we develop a prognostic signature to improve the stratification of high-risk stage II colon cancer patients., Method: RNA sequencing (RNA-Seq) data from 187 stage II colon cancer patients was obtained from the TCGA data portal. We excluded cases without a sufficient amount of survival data (n=21), leaving 166 stage II colon cancer patients to be selected for further survival analysis. Differentially expressed lncRNAs and miRNAs were unveiled by the edgeR package of R. A comprehensive ceRNAs regulatory network was constructed using the Cytoscape. Cox regression analysis was performed to screen prognostic RNAs and develop a prognostic signature. The Multi Experiment Matrix and Gene Ontology were undertaken to assess the prognostic lncRNA MIR31HG function., Results: The multivariate analysis indicates that 2 lncRNAs (WASIR2 and MIR31HG) and 2 miRNAs (hsa-mir-200a and hsa-mir-155) exhibited an independently significant prognostic value for stage II colon cancer. The 4 lncRNA-miRNA signatures for predicting the overall survival (OS) was constructed with the formula: Risk score=exp WASIR2*(0.213)+exp MIR31HG*(0.152)+exp hsa-mir-200a*(-0.329)+exp hsa-mir-155*(0.300). The area under the curve in the receiver operating characteristic analysis was 0.810. Kaplan-Meier survival curves confirm that the low-risk group had a low death rate, with a 5-year OS rate at 87.7%. However, the high-risk group had a low 5-year OS of 23.1% ( P =0.000). The correlative genes of MIR31HG were found to be enriched in the epithelial-to-mesenchymal transition pathway, and the VEGFR3 signaling in lymphatic endothelium pathways., Conclusions: These findings indicate that the 4 lncRNA-miRNA prognostic signature could be a marker for survival of stage II colon cancer patients., (© 2019 by the Association of Clinical Scientists, Inc.)