Circ_0084615 promotes epithelial-mesenchymal transition-mediated tumor progression in hepatocellular carcinoma

Aim

CircRNAs have been identified as crucial regulators in tumorigenesis and progression. This study aimed to explore the biological role and underlying mechanism of circ_0084615 in hepatocellular carcinoma (HCC).

Methods

The expression of RNAs was detected by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The effects of circ_0084615 silencing on malignant behaviors of HCC cells were assessed by CCK-8, colony formation, wound healing, and Transwell assays in vitro and tumor transplantation experiment in vivo. The expression of proteins was detected by Western blotting. Dual-luciferase reporter assay and RNA-binding protein immunoprecipitation were performed to explore the mechanism of circ_0084615.

Results

A significant upregulation of circ_0084615 was observed in HCC tissues, and positively correlated with the TNM staging. Silencing of circ_0084615 impeded HCC cell viability, colony formation, migration, invasion, epithelial-mesenchymal transition, and xenograft tumor growth. Mechanistically, circ_0084615 could bind to miR-1200 and eliminate its ability to destroy actin-like 6A (ACTL6A) mRNA, thereby increasing ACTL6A expression and facilitating the malignant behaviors of HCC cells.

Conclusions

This study clarified the oncogenic activity and mechanism of circ_0084615, thereby providing potential diagnostic biomarker and therapeutic target for inhibiting HCC progression.