Circ_0091579 Serves as a Tumor-Promoting Factor in Hepatocellular Carcinoma Through miR-1225-5p/PLCB1 Axis

Abstract

Hepatocellular carcinoma (HCC) is a dreadful threaten to human health worldwide. Many circular RNAs were reported to influence the malignant development of HCC. The aim of this study was to elucidate the role of circ_0091579 in HCC progression and the molecular fundamentation. Expression of circ_0091579, microRNA-1225-5p (miR-1225-5p), and phospholipase C, β1 (PLCB1) was examined by quantitative reverse transcription-polymerase chain reaction or Western blotting. Cell viability, clonogenicity capacity, and apoptosis were determined via Cell Counting Kit-8 assay, colony formation assay, and flow cytometry, respectively. Transwell assay was employed to detect cell migration and invasion. Target relationship between miR-1225-5p and circ_0091579 or PLCB1 was demonstrated by dual-luciferase reporter assay. Moreover, role of circ_0091579 in vivo was assessed by Xenograft model assay. Expression of circ_0091579 and PLCB1 was increased, while miR-1225-5p expression was decreased in HCC tissues and cells. Circ_0091579 or PLCB1 depletion had inhibitory effects on HCC cell proliferation and metastasis. Circ_0091579 sponged miR-1225-5p to upregulate PLCB1 expression in HCC cells. Silencing of miR-1225-5p contributed to HCC progression, which was mitigated by PLCB1 depletion. Circ_0091579 deficiency could suppress HCC tumor growth in vivo. Circ_0091579 knockdown repressed HCC progression and tumorigenesis by regulating miR-1225-5p/PLCB1 axis, affording a novel molecular basis for HCC development.