ArticleEuropean journal of medical research2025
KDM3B suppresses castration-resistance prostate cancer cell proliferation by promoting PTEN expression.
Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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1 citing paper in PubMed.
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6 authors.
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Abstract
backgroundCastration-resistant prostate cancer (CRPC) represents the terminal stage of prostate cancer (PCa), yet the molecular mechanisms driving its development remain unclear. Members of the histone lysine demethylase (KDM) family regulate histone methylation and thereby modulate transcriptional programs during malignant progression, contributing to PCa pathogenesis. While the function of KDM3B in PCa has been described, its involvement in CRPC remains uncertain. This study investigated the mechanistic role of KDM3B in CRPC progression.
methodsClinical specimens and publicly available datasets were analyzed to assess KDM3B expression in PCa and CRPC tissues. Cellular proliferation was evaluated through CCK-8 and colony formation assays. In addition, RT-PCR, WB, and CCK-8 assays were employed to elucidate the relationship between KDM3B activity and CRPC development.
resultsKDM3B expression was markedly reduced in both PCa and CRPC samples. Functional assays indicated that KDM3B suppressed the proliferative capacity of CRPC cells in vivo. Moreover, KDM3B upregulated PTEN expression, and its regulatory effect on CRPC cell proliferation was mediated through PTEN modulation.
conclusionThe findings suggest that KDM3B suppresses CRPC cell proliferation by enhancing PTEN expression, highlighting its potential role as a tumor-suppressive factor in PCa.
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