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.
Highlights
Cervical cancer (CC) is a malignancy that occurs in cervical cells, and causes high morbidity and mortality among females in China [1,2]
The cell experiment results indicated that Flap structure‐specific endonuclease 1 (FEN1) knockdown inhibited CC cell proliferation, migration and uncontrollable cell cycle progression, whereas miR‐140‐5p miR, microRNA; FEN1, flap structure‐specific endonuclease 1; NC, negative control; si, small interfering RNA
FEN1 promoted breast cancer cell proliferation by mediating DNA methyltransferase (DNMT)1 and DNMT3a to recover the expression of miR‐200a‐5p target genes [31]
Summary
Cervical cancer (CC) is a malignancy that occurs in cervical cells, and causes high morbidity and mortality among females in China [1,2]. In the early 1900s, the function of FEN1 was first identified and reported [15]. In the late 1990s, it was reported that FEN1 was downregulated during differentiation of the HL‐60 cell line (a human leukemia cell line) [17]. FEN1 upregulation has been identified as crucial for the maintenance of genome stability and for the progression of various malignancies occurring in prostate, lung, breast, brain, stomach and pancreatic tissues [20,21,22,23,24,25,26,27]. Previous studies have investigated the interaction between FEN1 and microRNAs (miRNAs/miRs) in human breast and hepatocellular cancer [29,30,31]. The interaction between FEN1 and miRNAs in CC is not completely understood
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
