MiR‑140‑5p inhibits cervical cancer cell phenotypes via downregulating FEN1 to halt the cell cycle.

Abstract

Cervical cancer (CC) is a frequently occurring cancer in women with a high mortality rate. Despite improvements to therapeutic strategies, the survival outcome for patients with CC remains poor. Therefore, the present study aimed to investigate the molecular mechanism underlying CC inhibition involving microRNA (miR)‑140‑5p and flap structure‑specific endonuclease1 (FEN1). Bioinformatics analysis was conducted, which identified that FEN1 was associated with CC cell cycle progression. Subsequently, 3'untranslated region reporter assays were performed to assess the regulatory relationship between FEN1 mRNA and miR‑140‑5p. Functional assays, including EdU staining assay, flow cytometry, and wound healing assays, were conducted to observe CC cell phenotypes induced by alterations to miR‑140‑5p and FEN1 expression levels. FEN1 expression was high and miR‑140‑5p expression was low in CC tissues and cell lines compared with adjacent healthy tissues and a normal cervical epithelial cell line, respectively. miR‑140‑5p knockdown reversed small interfering RNA‑FEN1‑mediated suppressive effects on CC cell phenotypes, potentially via inducing cell cycle arrest at the G1phase. Therefore, the present study suggested that miR‑140‑5p may serve as an antitumorigenesis factor in CC by targeting FEN1 mRNA.