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Translation regulatory long non-coding RNA 1 (TRERNA1) sponges microRNA-23a to suppress granulosa cell apoptosis in premature ovarian failure.

ABSTRACT: Translation regulatory long non-coding RNA 1 (TRERNA1) plays critical roles in cancer biology. We predicted the direct interaction of TRERNA1 with microRNA (miR)-23a, which promotes granulosa apoptosis. Granulosa apoptosis is involved in premature ovarian failure (POF). This study was therefore carried out to explore the involvement of TRERNA1 and miR-23a in POF. The expression of TRERNA1 and miR-23a in POF and control groups were detected by RT-qPCRs. The subcellular locations of TRERNA1 in granulosa cell line COV434 was detected by subcellular fractionation assay. The interaction between TRERNA1 and miR-23a was predicted using IntaRNA2.0. The direct interaction between COV434 and miR-23a was explored with RNA pull-down assay. In granulosa cells, the direct interaction between TRERNA1 and miR-23a was verified by overexpression assay. Cell apoptosis assay was performed to evaluate cell apoptosis. Both TRERNA1 and miR-23a were downregulated in POF. In addition, TRERNA1 was detected in both cytoplasm and nuclear samples of granulosa cells, and directly interacted with miR-23a. TRERNA1 did not affect the expression of miR-23a in granulosa cells, while TRERNA1 suppressed the role of miR-23a in enhancing cell apoptosis. In conclusion, TRERNA1 may sponge miR-23a to suppress granulosa cell apoptosis in POF.

SUBMITTER: Zhang L

PROVIDER: S-EPMC8973726 | biostudies-literature | 2022 Feb

REPOSITORIES: biostudies-literature

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Translation regulatory long non-coding RNA 1 (TRERNA1) sponges microRNA-23a to suppress granulosa cell apoptosis in premature ovarian failure.

Zhang Lili L Mao Bin B Zhao Xiaodong X Yuan Yue Y Wang Wei W Lin Shaohua S

Bioengineered 20220201 2

Translation regulatory long non-coding RNA 1 (TRERNA1) plays critical roles in cancer biology. We predicted the direct interaction of TRERNA1 with microRNA (miR)-23a, which promotes granulosa apoptosis. Granulosa apoptosis is involved in premature ovarian failure (POF). This study was therefore carried out to explore the involvement of TRERNA1 and miR-23a in POF. The expression of TRERNA1 and miR-23a in POF and control groups were detected by RT-qPCRs. The subcellular locations of TRERNA1 in gra ...[more]

PMID: 35034562

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Project description:BackgroundPremature ovarian insufficiency (POI) is a condition characterized by a substantial decline or loss of ovarian function in women before the age of 40. However, the pathogenesis of POI remains to be further elucidated, and specific targeted drugs which could delay or reverse ovarian reserve decline are urgently needed. Abnormal DNA damage repair (DDR) and cell senescence in granulosa cells are pathogenic mechanisms of POI. Ubiquitin-specific protease 14 (USP14) is a key enzyme that regulates the deubiquitylation of DDR-related proteins, but whether USP14 participates in the pathogenesis of POI remains unclear.MethodsWe measured USP14 mRNA expression in granulosa cells from biochemical POI (bPOI) patients. In KGN cells, we used IU1 and siRNA-USP14 to specifically inhibit USP14 and constructed a cell line stably overexpressing USP14 to examine its effects on DDR function and cellular senescence in granulosa cells. Next, we explored the therapeutic potential of IU1 in POI mouse models induced by D-galactose.ResultsUSP14 expression in the granulosa cells of bPOI patients was significantly upregulated. In KGN cells, IU1 treatment and siUSP14 transfection decreased etoposide-induced DNA damage levels, promoted DDR function, and inhibited cell senescence. USP14 overexpression increased DNA damage, impaired DDR function, and promoted cell senescence. Moreover, IU1 treatment and siUSP14 transfection increased nonhomologous end joining (NHEJ), upregulated RNF168, Ku70, and DDB1, and increased ubiquitinated DDB1 levels in KGN cells. Conversely, USP14 overexpression had the opposite effects. Intraperitoneal IU1 injection alleviated etoposide-induced DNA damage in granulosa cells, ameliorated the D-galactose-induced POI phenotype, promoted DDR, and inhibited cell senescence in ovarian granulosa cells in vivo.ConclusionsUpregulated USP14 in ovarian granulosa cells may play a role in POI pathogenesis, and targeting USP14 may be a potential POI treatment strategy. Our study provides new insights into the pathogenesis of POI and a novel POI treatment strategy.

Dataset Information

Translation regulatory long non-coding RNA 1 (TRERNA1) sponges microRNA-23a to suppress granulosa cell apoptosis in premature ovarian failure.

Publications

Translation regulatory long non-coding RNA 1 (TRERNA1) sponges microRNA-23a to suppress granulosa cell apoptosis in premature ovarian failure.

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