Circ_0005050 promotes the proliferation of oral squamous cell carcinoma and inhibits the apoptosis by activating JAK/STAT3 signaling pathway

Pathol Res Pract. 2022 Oct:238:154058. doi: 10.1016/j.prp.2022.154058. Epub 2022 Aug 4.

Abstract

Oral squamous cell carcinoma (OSCC) is the most predominant type of oral cancer, featured with poor prognosis and high mortality. Circular RNA (circRNA) exerts its function in a variety of human cancers, including OSCC. Circ_0005050, as a novel circRNA, has not been well explored in OSCC so far. This study centered on investigating the impact of circ_0005050 on OSCC cell growth and its molecular mechanism. RNA or protein expression was detected by RT-qPCR or western blot analysis. Functional assays were employed to uncover the changes of OSCC cell biological behaviors. Mechanistic assays were done to verify the underlying mechanism of circ_0005050 in OSCC cells. According to the collected data, circ_0005050 was significantly up-regulated in OSCC cells compared to normal cells. Circ_0005050 depletion hampered proliferative ability of OSCC cells while promoting cell apoptotic ability. As for mechanism analyses, circ_0005050 knockdown led to the reduction of STAT3 expression and JAK/STAT3 signaling pathway activity. Moreover, circ_0005050 competitively bound to miR-23a-3p and miR-625-5p to up-regulate STAT3, thus prompting malignant behaviors of OSCC cells. In conclusion, circ_0005050 regulates miR-23a-3p/miR-625-5p/STAT3 axis to activate JAK/STAT3 signaling pathway, consequently facilitating OSCC cell proliferation and inhibiting cell apoptosis.

Keywords: Circ_0005050; JAK/STAT3; MiR-23a-3p; MiR-625–5p; Oral squamous cell carcinoma.