The expression and clinical significance of miRNA-182 in patients with colorectal cancer

JIANG Ya-ping; CAI Sha-sha; LIAO Nan-sheng

doi:10.13820/j.cnki.gdyx.20244031

Abstract：Objective To investigate the expression and clinical significance of microRNA-182(miRNA-182)in patients with colorectal cancer(CRC)and CRC cell lines.Methods A total of 65 CRC patients admitted be-tween January 2019 and December 2023 were enrolled as the study group,with 65 healthy individuals undergoing physical examinations during the same period serving as the control group.The expression levels of miRNA-182 were assessed by quantitative real-time PCR(qRT-PCR)in patient tissues and various CRC cell lines.Cellular viability was evaluated after miRNA-182 knockdown or overexpression.Results miRNA-182 expression was significantly upregulated in CRC tissues compared to the control group(t=11.227,21.441,P＜0.05).Its expression was significantly associated with TNM stage,lymph node metastasis,and tumor differentiation(t=7.609,8.078,6.485,P＜0.05).Receiver operating characteristic(ROC)curve analysis showed that miRNA-182 had a high diagnostic accuracy for CRC,with an AUC of 0.934.Kaplan-Meier survival analysis indicated that patients with low miRNA-182 expression had significantly better cumulative survival rates than those with high expression.Multivariate Cox regression analysis identified TNM stage,tumor differentiation,lymph node metastasis,and miRNA-182 expression as independent prognostic factors(P＜0.05).In CRC cell lines,miRNA-182 was markedly upregulated compared to normal intestinal epithelial cells.Knockdown of miRNA-182 reduced cell viability and increased the expression of apoptosis-related protein cleaved-PARP1(C-PARP1)and the autophagy marker LC3 Ⅱ.Conversely,overexpression of miRNA-182 enhanced cell viability while sup-pressing C-PARP1 and LC3 Ⅱ expression.Conclusion miRNA-182 is significantly upregulated in colorectal cancer and serves as an oncogenic miRNA and independent risk factor.It may promote CRC progression by modulating autophagy-related signaling pathways.