LINC00657 promotes the development of colon cancer by activating PI3K/AKT pathway.

Abstract

The aim of this study was to explore whether LINC00657 can regulate cell proliferation and invasion by regulating the PI3K/AKT pathway and thus participate in the occurrence of colon cancer. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was applied to detect the expression levels of LINC00657 and E-cad in colon cancer tissues and corresponding adjacent tissues obtained from 80 patients, and the correlation was analyzed between LINC00657 expression and clinical information of patients such as prognosis, tumor size, tumor stage, and distant metastasis. The expression of LINC00657 and E-cad in colon cancer cell lines was also examined, and the effect of LINC00657 on tumor cell proliferation was evaluated by cell counting kit-8 (CCK-8) assay and colony formation experiments. Meanwhile, transwell assay was performed to evaluate the influence of LINC00657 and CAPN7 on cell invasive ability. In addition, the effect of LINC00657 on CAPN7 and PI3K/AKT pathway was detected by Western blot assay. The expression levels of LINC00657 and E-cad in tumor tissues decreased remarkably, especially in patients who occurred distant metastasis. Compared with patients with highly-expressed LINC00657, the patients with lower level of LINC00657 had a worse prognosis and an advanced tumor size and TNM stage. Similarly, LINC00657 and E-cad also showed a decrease in colon cancer cell lines. After overexpression of LINC00657, cell viability and invasive ability decreased remarkably while cell apoptosis rate increased significantly. In addition, high expression of LINC00657 in an in vitro model significantly promoted CAPN7 expression and inhibited activation of PI3K/AKT pathway. LINC00657 had a low expression in colon cancer tissues, which could accelerate cell proliferation and invasion by activating PI3K/AKT pathway and inhibiting CAPN7 expression.