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Long non-coding RNA NEAT1 promotes ovarian granulosa cell proliferation and cell cycle progression via the miR-29a-3p/IGF1 axis

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机构: [1]Department of Reproductive Medicine, Zigong Hospital of Women and Children Health Care, Zigong, Sichuan, China. [2]Department of Urology, Zigong Fourth People's Hospital, Zigong, Sichuan, China. [3]Institute of Precision Medicine, Zigong Academy of Big Data and Artificial Intelligence for Medical Science, Zigong, Sichuan, China. [4]Department of Urology, Institute of Science Tokyo, 1-5-45 Yushima, Bunkyo- ku, Tokyo, Japan.
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关键词: Long non-coding RNA NEAT1 miR-29a-3p IGF1 Granulosa cells

摘要:
Granulosa cell proliferation and survival are essential for normal ovarian function and follicular development. Long non-coding RNAs (lncRNAs) have emerged as important regulators of cell proliferation and differentiation. Nuclear paraspeckle assembly transcript 1 (NEAT1) has been implicated in various cellular processes, but its role in granulosa cell function remains unclear.We investigated the function of lncRNA NEAT1 in human ovarian granulosa-like tumor cells (KGN). The effects of NEAT1 overexpression or silencing on cell proliferation and cell cycle were evaluated using CCK-8 assays and flow cytometry. The interaction between NEAT1, miR-29a-3p, and IGF1 was examined using dual-luciferase reporter assays, qRT-PCR, and Western blot analysis.NEAT1 promoted granulosa cell proliferation and cell cycle progression by indirectly upregulated IGF1 expression through acting as a molecular sponge for miR-29a-3p. Cell proliferation and G2/M phase proportions were increased by overexpression of NEAT1, whereas cell proliferation and G2/M phase proportions decreased with NEAT1 silencing. The effects of NEAT1 on cell proliferation and cell cycle-related proteins (CCNB1 and CDK2) were partially reversed by miR-29a-3p mimic, while miR-29a-3p inhibitor rescued the effects of NEAT1 silencing.LncRNA NEAT1 could promote ovarian granulosa cell proliferation and cell cycle progression via the miR-29a-3p/IGF1 axis in polycystic ovary syndrome. Further investigation of this mechanism in clinical samples may have implications for understanding ovarian physiology and pathology.© 2025. The Author(s).

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大类 | 3 区 医学
小类 | 3 区 生殖生物学
第一作者:
第一作者机构: [1]Department of Reproductive Medicine, Zigong Hospital of Women and Children Health Care, Zigong, Sichuan, China.
通讯作者:
通讯机构: [2]Department of Urology, Zigong Fourth People's Hospital, Zigong, Sichuan, China. [3]Institute of Precision Medicine, Zigong Academy of Big Data and Artificial Intelligence for Medical Science, Zigong, Sichuan, China. [4]Department of Urology, Institute of Science Tokyo, 1-5-45 Yushima, Bunkyo- ku, Tokyo, Japan.
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