Circ_0085616 contributes to the radio-resistance and progression of cervical cancer by targeting miR-541-3p/ARL2 signaling

Circular RNAs (circRNAs) play crucial regulatory roles in cancer progression and the development of radio-resistance. Here, we intended to explore the role of circ_0085616 in cervical cancer progression and its associated mechanism.

Circ_0085616 contributed to the radio-resistance and progression of cervical cancer partly through mediating the miR-541-3p/ARL2 axis.

Colony formation assay was employed to analyze the radio-resistance and proliferation of cervical cancer cells. Cell proliferation ability was also assessed by 5-ethynyl-2'-deoxyuridine (EdU) assay. Cell apoptosis was analyzed by flow cytometry. Tube formation assay was performed to analyze cell angiogenesis ability. Transwell assays were conducted to measure cell migration and invasion abilities. Dual-luciferase reporter assay was utilized to verify the target relationships. Xenograft mice model was used to analyze the role of circ_0085616 in tumor growth in vivo.

Circ_0085616 expression was elevated in cervical cancer tissues and cell lines. Circ_0085616 interference suppressed the radio-resistance, proliferation, tube formation, migration, and invasion and elevated the apoptosis rate of cervical cancer cells. Circ_0085616 acted as a sponge for microRNA-541-3p (miR-541-3p), and miR-541-3p was negatively regulated by circ_0085616 in cervical cancer cells. Circ_0085616 absence-induced changes in the behaviors of cervical cancer cells were largely overturned by anti-miR-541-3p. miR-541-3p negatively regulated ADP ribosylation factor like GTPase 2 (ARL2) expression by binding to its 3' untranslated region (3'UTR). miR-541-3p mimic-induced effects were largely reversed by pcDNA-ARL2 in cervical cancer cells. Circ_0085616 positively regulated ARL2 expression by sequestering miR-541-3p. Circ_0085616 absence significantly inhibited the tumor growth in vivo.