ArticleCytotechnology2025
KDM1A-mediated ZFP64 demethylation activates CENPL to promote epithelial ovarian cancer progression.
Article in Cytotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Review
- Discovery and structural studies of histone demethylases.Frontiers in epigenetics and epigenomics · 2025Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lysine-specific histone demethylase 1A (KDM1A) has emerged as an attractive therapeutic target for treating various cancers, owing to its observed overexpression. However, its function in epithelial ovarian cancer (EOC) remains uncertain. The current study sought to investigate the function of KDM1A on malignant phenotypes of EOC cells as well as the underlying mechanism. Colony formation assay, cell counting kit-8, wound healing, Transwell assays, and TUNEL assays were performed to investigate the effects of KDM1A, Zinc finger protein 64 (ZFP64), and centromere protein L (CENPL) in vitro, while subcutaneous tumor formation models were established in nude mice to evaluate their roles in vivo. KDM1A, ZFP64, and CENPL were overexpressed in EOC tissues and cells. Knockdown of KDM1A, ZFP64, or CENPL inhibited the biological behavior of EOC cells. In addition, chromatin immunoprecipitation showed that KDM1A stimulated ZFP64 expression by removing the H3K9me2 mark from its promoter. Restoration of ZFP64 promoted EOC cell malignant phenotype in the presence of KDM1A knockdown. ZFP64 activated CENPL transcription. Reactivation of CENPL promoted the growth of EOC cells in vivo inhibited by knockdown of ZFP64. Collectively, KDM1A promoted EOC cell proliferation, migration, and invasion, and reduced apoptosis by activating the ZFP64/CENPL axis, which triggered EOC progression. Supplementary Information: The online version contains supplementary material available at 10.1007/s10616-024-00671-w.
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