MicroRNA‑601 serves as a potential tumor suppressor in hepatocellular carcinoma by directly targeting PIK3R3.

Recently, microRNAs (miRNAs) have been acknowledged as important regulators of hepatocarcinogenesis and tumor progression. Therefore, identifying the underlying molecular mechanisms of miRNAs in the occurrence and development of hepatocellular carcinoma (HCC) may be important for understanding the pathogenesis of HCC and aid the identification of potential therapeutic strategies. In the present study, miRNA (miR)‑601 was significantly downregulated in HCC tissues and cell lines; low miR‑601 expression was strongly associated with tumor, node and metastasis staging and lymph node metastasis of patients with HCC. In addition, the overexpression of miR‑601 expression significantly inhibited the proliferation and invasion of HCC cells. Regarding the underlying mechanism, phosphoinositide‑3‑kinase regulatory subunit 3 (PIK3R3) was predicted to be a direct target of miR‑601 in HCC cells. Furthermore, restoration of PIK3R3 expression in these cells counteracted the inhibitory effects of miR‑601 on cell proliferation and invasion in HCC. Notably, miR‑601 overexpression inhibited the protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway in HCC via the regulation of PIK3R3. Collectively, these results demonstrated that miR‑601 may inhibit the progression of HCC by directly targeting PIK3R3 and regulating the AKT/mTOR signaling pathway. Therefore, miR‑601 may be an effective therapeutic target for the treatment of patients with HCC.