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

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

Abstract Background 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 bee...

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Bibliographic Details
Main Authors: Lina He, Jie Lin, Zhengwen Qin, Qing Xu, Li Hao, Yanhong Fu, Xu Ran, Wei Chen
Format: Article
Language:English
Published: BMC 2025-01-01
Series:Journal of Ovarian Research
Subjects:
Long non-coding RNA
NEAT1
miR-29a-3p
IGF1
Granulosa cells
Online Access:https://doi.org/10.1186/s13048-025-01588-4
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Summary:Abstract Background 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. Methods 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. Results 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. Conclusion 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.
ISSN:1757-2215

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