CircAGFG1 aggravates the progression of cervical cancer by downregulating p53.

Abstract

To explore the role of circAGFG1 in influencing the progression of cervical cancer (CC) and the underlying molecular mechanism. CircAGFG1 levels in CC tissues and paracancerous tissues were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Its level in CC cell lines was detected as well. Meanwhile, circAGFG1 levels in CC patients with different tumor staging, metastatic statues, and tumor sizes were examined. The Kaplan-Meier method was introduced for assessing the prognostic potential of circAGFG1 in CC. The regulatory effects of circAGFG1 on the proliferative ability of CC cells were evaluated by performing the Cell Counting Kit-8 (CCK-8) and 5-Ethynyl-2'-deoxyuridine (EdU) assay. The subcellular distribution of circAGFG1 in the CC cells was analyzed. Through chromatin immunoprecipitation (ChIP) and RNA immunoprecipitation (RIP) assay, the interaction between circAGFG1 and p53 was determined. Finally, the role of the circAGFG1/p53 axis in influencing the proliferation of CC cells was uncovered. CircAGFG1 was upregulated in CC tissues and cell lines. Besides, the circAGFG1 level was closely related to worse tumor staging, a higher rate of metastasis, and larger tumor size in CC patients. Besides, CC patients with a high level of circAGFG1 presented worse prognosis. The knockdown of circAGFG1 attenuated the proliferative ability of SiHa and HeLa cells. CircAGFG1 was mainly distributed in the nucleus of the CC cells. The interaction between circAGFG1 and p53 was verified. The knockdown of p53 could partially reverse the regulatory effect of circAGFG1 on the proliferative ability of the CC cells. CircAGFG1 is upregulated in CC. By recruiting EZH2, circAGFG1 downregulates p53 and thus exerts a carcinogenic role to accelerate the malignant progression of cervical cancer.