MicroRNA‑133a and microRNA‑326 co‑contribute to hepatocellular carcinoma 5‑fluorouracil and cisplatin sensitivity by directly targeting B‑cell lymphoma‑extra large.

Chemotherapy is one of the most common treatments used for hepatocellular carcinoma (HCC), which effectively improves outcome and reduces tumor recurrence. However, the drug resistance mechanisms involved in chemotherapy, which is the predominant challenge in HCC treatment, remain to be fully elucidated. Therefore, there is an urgent requirement for the identification of novel therapeutic strategies or drugs. MicroRNAs (miRs) have become an area of interest, and in the present study, the effects of miR‑133a and miR‑326 on HepG2 cells, and their function on B‑cell lymphoma‑extra large (Bcl‑xl) in HepG2 cells were investigated. Using computational programs, Bcl‑xl was predicted as the common target gene of miR‑133a and miR‑326. A dual‑luciferase reporter assay was used to verify the target genes of miRs. The mRNA and protein levels of Bcl‑xl were observed to be downregulated following transfection with miR‑133a or miR‑326 mimics. Combining miR‑133a or miR‑326 with 5‑fluorouracil (5‑FU) or cisplatin (DDP) resulted in increased cell death. The results of the present study indicated that miR‑133a, miR‑326 and Bcl‑xl acted protectively against the apoptosis, induced by 5‑FU or DDP, in HepG2 cells. This suggested the potential use of miRs either as ancillary anti‑cancer drugs or as anti‑cancer drugs themselves.