Journal
EBIOMEDICINE
Volume 36, Issue -, Pages 526-538Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ebiom.2018.09.043
Keywords
Polycystic ovary syndrome; IncRNA; Granulosa cells; Proliferation
Funding
- National Key Research and Development Program of China [2017YFC1001002]
- National Natural Science Foundation [81490743, 81671413, 81671414]
- National Institutes of Health [1R01HD085527]
- Shanghai Municipal Education Commission-Gaofeng Clinical Medicine [20152510]
- Shanghai Key Laboratory for Assisted Reproduction and Reproductive Genetics [17DZ2271100]
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Background: Disordered folliculogenesis is a key feature of polycystic ovary syndrome (PCOS), but the underlying molecular mechanism remains unclear. Methods: Long non-coding RNA (IncRNA) expression in luteinized granulosa cells (hLGCs) derived from women with and without PCOS were analyzed using microarray and qRT-PCR. Immortalized human granulosa cell lines were cultured for proliferation assays after transfection with the LINC-01572:28 over-expression vector in the presence or absence of p27 siRNA. Protein expression analysis, rescue assays, and RNA immunoprecipitation (RIP) were used to confirm the LINC-01572:28 substrate. Findings: LINO-01572:28 and p27 protein were elevated whereas proliferating cell nuclear antigen protein was decreased in the hLGCs of women with PCOS. LINC-01572:28 expression was positively correlated with basal testosterone levels. Over-expression of LINC-01572:28 inhibited cell proliferation and impeded G1/S transition, which were partially reversed by siRNA-mediated p27 knockdown. Interpretation: Our findings, therefore, suggest that LINC-01572:28 suppresses cell proliferation and cell cycle progression by reducing the degradation of p27 protein via SKP2 binding. (C) 2018 The Authors. Published by Elsevier B.V.
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