Colorectal cancer (CRC) is one of the most common malignancies and has been a leading cause of cancer-related death worldwide in recent years. N6-methyladenosine (m6A) methylation is the most abundant epigenetic modification of various types of RNAs, and it plays a vital role in promoting cancer development. Here, we obtained SNV and transcriptome data of CRC from The Cancer Genome Atlas (TCGA). We demonstrated that most m6A methylation regulators were aberrantly expressed in individuals with CRC. The abnormal expression of m6A regulators was caused by their different copy number variation (CNV) patterns, and alteration of m6A regulators was significantly correlated with prognosis and tumor stage. By using weighted coexpression network analysis (WGCNA), we identified m6A-related long noncoding RNAs (lncRNAs) and mRNAs; then we used least absolute shrinkage and selection operator (LASSO) Cox regression analysis to construct m6A-related lncRNA and mRNA prognostic signatures in the TCGA dataset. Furthermore, a nomogram with clinicopathological features, lncRNA risk scores, and mRNA risk scores was established, which showed a strong ability to forecast the overall survival of the individuals with CRC in training and testing sets. In conclusion, m6A methylation regulators played a vital role in affecting the prognosis of subjects with CRC, and m6A-related lncRNAs and mRNAs revealed underlying mechanisms in CRC tumorigenesis and progression.

Background:The purpose of this study was to compare the efficacy and safety of laparoscopic cholecystectomy (LC) plus laparoscopic common bile duct (CBD) stones exploration (LCBDE) with LC plus endoscopic sphincterotomy (EST) in the treatment of patients with gallstones and CBD stones.Methods:The authors searched PubMed, Web of Science, and Embase to identify relevant studies. Risk ratios (RRs) were pooled to compare stone clear, retained stone, conversion to other procedures, and complications. Weighted mean differences (WMDs) were pooled to compare operative time, and length of hospital stay. A fixed-effects model or random-effects model was used to pool the estimates, according to the heterogeneity among the included studies.Results:A total of 11 randomized controlled trials (RCTs) involving 1663 patients were included in this meta-analysis. The pooled estimate suggested that LC-LCBDE had comparable effects with LC-EST in terms of CBD stone clear rate (RR = 1.02, 95% CI: 0.95, 1.09; P = .583), retained stones rate (RR = 1.27, 95% CI: 0.51, 3.19; P = .607), and length of hospital stay (WMD = −0.96 days, 95% CI: −2.20, 0.28). In addition, LC-LCBDE was associated with significantly higher conversion rate (RR = 1.59, 95% CI: 1.08, 2.35; P = .019) and less operative time (WMD = −11.55 minutes, 95% CI: −16.68, −6.42; P < .001) than LC-EST. The incidence of complications was not significant difference between the 2 surgical approaches (RR = 1.07, 95% CI: 0.86, 1.34; P = .550).Conclusion:Based on the current evidence, both LC-LCBDE and LC-EST were highly effective in detecting and removing CBD stones and were equivalent in complications. However, our results might be biased by the limitations. Large-scale well-designed RCTs are needed to confirm our findings.

Cysteine-rich protein 61 (CYR61) and metastasis associated in colon cancer (MACC1) protein promoted human colorectal cancer (CRC) cell metastasis and closely related to the patient's prognosis in colorectal cancer. The purpose of this article is to investigate whether CYR61 and MACC1 can serve as dual potential targets for gene therapy of human CRC. In this study, microRNA (miRNA) targeting for both CYR61 and MACC1 was used to investigate the mechanism and therapeutic effects for CRC cells and mice with CRC. We observed that silencing miRNA for CYR61 and MACC1 inhibited the epithelial-mesenchymal transition (EMT) process, and co-treatment strengthened this effect. MTT assay showed that the growth of colorectal tumor cells was decreased due to miRNA treatment. Apoptosis assay revealed that miRNA for CYR61 and MACC1 promoted CRC cells apoptotic. The animals' study results showed that the expression levels of CYR61 and MACC1 were significantly decreased after miRNA-100 and miRNA-143 treatment, respectively. The expression levels of apoptosis-promoting protein were increased significantly after treatment with miRNA-100 and miRNA-143, which suggested that both miRNA-100 and miRNA-143 may induce apoptosis by mitochondria-dependent pathway. In addition, metastasis and invasion assays showed that miRNA-100 and miRNA-143 treatment inhibited obviously migratory and invasive abilities of CRC cells. Furthermore, our data also showed that the tumor growth was significantly inhibited and survival rate of tumor-bearing mice was greatly improved by common treatments of miRNA-100 and miRNA-143. In conclusion, the abilities of apoptosis, metastasis, and invasion in CRC tumor cells were significantly suppressed by miRNA-100 and miRNA-143 targeting CYR61 and MACC1, respectively. As a result, CYR61 and MACC1 may serve as potential targets for gene therapy in human CRC treatments.