MicroRNA‑212 inhibits colorectal cancer cell viability and invasion by directly targeting PIK3R3.

Abstract

Colorectal cancer (CRC) is the third most common cancer and the fourth most common cause of cancer‑associated mortalities worldwide. Emerging evidence has shown that abnormal microRNA (miRNA) expression contributes to CRC carcinogenesis and progression by inhibiting the expression of their target genes. Therefore, investigating the expression patterns and roles of miRNAs specifically involved in CRC formation, and progression would help expand our knowledge on CRC and provide novel therapeutic targets for CRC treatment. Previous studies suggest that miR‑212 is involved in the carcinogenesis and progression of multiple human cancer types. In this study, miR‑212 was significantly downregulated in CRC tissues and cell lines. Functional experiments demonstrated that miR‑212 overexpression inhibited the invitro viability and invasion of CRC cells. In addition, phosphoinositide‑3‑kinase regulatory subunit 3 (PIK3R3) was confirmed as the direct target of miR‑212 in CRC. Furthermore, PIK3R3 was highly expressed in CRC tissues and inversely correlated with miR‑212 expression. Increased PIK3R3 expression effectively rescued the tumor‑suppressing roles of miR‑212 on CRC cell viability and invasion. Moreover, miR‑212 upregulation blocked the protein kinaseB (AKT)/mechanistic target of rapamycin (mTOR) signalling pathway in CRC cells. These findings suggest that miR‑212 acts as a tumor suppressor in CRC by directly targeting PIK3R3 and regulating the AKT/mTOR signaling pathway. Thus, miR‑212 may serve as an effective therapeutic target for the treatment of patients with CRC.