LINC02418 promotes colon cancer progression by suppressing apoptosis via interaction with miR-34b-5p/BCL2 axis

Abstract

Background LncRNAs have been demonstrated to be functional regulators in tumor progression through interaction with various signaling pathways in multiple cancer types. However, the effect of LINC02418 on CRC progression still remains unclear. Methods LncRNA expression profile in CRC tissues was explored by using the TCGA database. The expressional level of LINC02418 in CRC patients was confirmed by qRT-PCR. Kaplan-Meier analyses was used to investigate the correlations between LINC02418 and OS of patients with CRC. After stably transducing sh-LINC02418 and sh-NC into HCT116 and LoVo cells, cell proliferative, migratory and invasive abilities were detected by CCK-8 assay, colony formation assay and trans-well assay, respectively. The binding between LINC02418 and miR-34b-5p, and the interaction between miR-34b-5p and BCL2 were determined by dual-luciferase assay. Western blot experiments were conducted to further explore the effect of miR-34b-5p on BCL2 signaling pathway. Rescue experiments were performed to uncover the role of LINC02418 /miR-34b-5p/ BCL2 axis in CRC progression. Results LINC02418 was upregulated in human colon cancer samples and its high expression correlated with poor prognosis. LINC02418 promoted cancer progression by enhancing tumor growth, cell mobility and invasiveness of colon cancer cells. Additionally, LINC02418 could physically bind to miR-34b-5p and subsequently interact with BCL2 signaling pathway. Down-regulation of LINC02418 reduced cell proliferation, but transfection of miR-34b-5p inhibitor or BCL2 in LINC02418-silenced colon cancer cells significantly promoted cell growth. Conclusions LINC02418 was upregulated in human colon cancer samples and could be used as indicator for prediction of prognosis. LINC02418 acted as a tumor driver by negatively regulating cell apoptosis through LINC02418 /miR-34b-5p/ BCL2 axis and in colorectal cancer.

miR-34b-5p promotes renal cell inflammation and apoptosis by inhibiting aquaporin-2 in sepsis-induced acute kidney injury

“…For instance, miR-34b-5p was induced by p53 to block NF-jB-inducing kinase and therefore inhibit noncanonical NF-jB signaling [22]. Overexpression of miR-34b-5p promoted tumor cell apoptosis in serval cancers, including thyroid carcinoma [23], colorectal cancer [24], and oral cancer [25]. Also, miR-34b-5p mediated recurrent seizures-induced apoptosis of hippocampal astrocytes [9].…”

Expression characteristics of long non-coding RNA in colon adenocarcinoma and its potential value for judging the survival and prognosis of patients: bioinformatics analysis based on The Cancer Genome Atlas database

“…It was found that expression of CRNDE was abnormally increased in tumors, and the KM survival analysis plot revealed that it was closely related to the prognosis of cancer patients. In the study by Tian et al (24), LINC02418 expression was found to be up-regulated in human colon cancer samples compared with adjacent tissues, and its high expression level was associated with poor prognosis of CRC patients and could be used as an indicator to predict prognosis. The results of another study (25) suggested that BLACAT1, as a cell cycle regulator, may be a potential target for the prevention and treatment of human colon cancer.…”