Long non-coding RNA HLA-F antisense RNA 1 inhibits the maturation of microRNA-613 in polycystic ovary syndrome to promote ovarian granulosa cell proliferation and inhibit cell apoptosis
- PMID: 35603775
- PMCID: PMC9275988
- DOI: 10.1080/21655979.2022.2070965
Long non-coding RNA HLA-F antisense RNA 1 inhibits the maturation of microRNA-613 in polycystic ovary syndrome to promote ovarian granulosa cell proliferation and inhibit cell apoptosis
Abstract
MicroRNA-613 (miR-613) inhibits granulosa cell proliferation, suggesting its involvement in polycystic ovary syndrome (PCOS). We predicted that long non-coding RNA (lncRNA) HLA-F antisense RNA 1 (HLA-F-AS1) could interact with premature miR-613. We then explored the crosstalk between HLA-F-AS1 and miR-613 in PCOS. In this study, follicular fluid donated by 58 healthy controls and 58 PCOS patients was used to analyze the expression of HLA-F-AS1 and miR-613 (mature and premature). The direct interaction between HLA-F-AS1 and premature miR-613 was evaluated by RNA pull-down assay. Overexpression of both HLA-F-AS1 and miR-613 was achieved in granulosa cells to assess their interactions. Cell proliferation and apoptosis were detected with BrdU assay and cell apoptosis assay, respectively. We found that miR-613 was highly expressed in PCOS, while HLA-F-AS1 was downregulated in PCOS. HLA-F-AS1 directly interacted with premature miR-613, and overexpression of HLA-F-AS1 increased the expression levels of premature miR-613, but decreased the expression levels of mature miR-613. HLA-F-AS1 increased ovarian granulosa cell proliferation and inhibited cell apoptosis. MiR-613 played an opposite role and suppressed the role of HLA-F-AS1. Therefore, HLA-F-AS1 may inhibit the maturation of miR-613 in PCOS to promote ovarian granulosa cell proliferation and inhibit cell apoptosis.
Keywords: HLA-F-AS1; Polycystic ovary syndrome; apoptosis; miR-613; proliferation.
Conflict of interest statement
No potential conflict of interest was reported by the author(s).
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