KDM4B overexpression

Tumour cells with high KDM4B expression exhibited higher CNV levels and a greater proportion of cells in the G1/S transition phase. Our results confirm that KDM4B promotes the progression of clear cell renal carcinoma, is correlated with poor prognosis, and may be related to high levels of CNV and cell cycle progression.

B3 suppressed the growth of 22Rv1 xenografts and sensitized tumor to anti-androgen receptor (AR) antagonist enzalutamide inhibition. B3 also inhibited 22Rv1 tumor growth synergistically with rapamycin, leading to cell apoptosis...Our studies establish KDM4B as a target for CRPC and B3 as a potential therapeutic agent. B3 as monotherapy or in combination with other anti-PCa therapeutics offers proof of principle for the clinical translation of epigenetic therapy targeting KDMs for CRPC patients.

KDM4B may be a new potential oncogene that is clinically significant in patients with UCEC. KDM4B may not only be used to assess the clinical prognosis of patients with UCEC but may also be a target for immunotherapy or targeted gene therapy.

Kaplan-Meier plots suggest that elevated KDM4B expression may contribute to a better or worse prognosis in a manner specific to each cancer type. Overall, our findings suggest that KDM4B plays complex roles in regulating multiple cancer processes, providing a useful resource for the future development of cancer therapies that target KDM4B expression.

This study evidenced that miR-545 suppresses progression of OC through mediating PLK1 expression by a direct binding and an indirect regulation involving KDM4B-mediated demethylation.

Here we found that KDM4B is overexpressed in enzalutamide-resistant prostate cancer cells...Clinically, KDM4B expression was found upregulated and to correlate with prostate cancer progression and poor prognosis. Our results revealed a novel mechanism of anti-androgen resistance via histone demethylase alteration which could be targeted through inhibition of KDM4B to reduce AR dependent-c-Myc expression and overcome resistance to AR-targeted therapies.