ArticleClinical and translational medicine2025
EHMT2-mediated R-loop formation promotes the malignant progression of prostate cancer via activating Aurora B.
Article in Clinical and translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Protein modification systems as cancer biomarkers and therapeutic targets.Precision clinical medicine · 2026Review
- Targeting EHMT2 inhibition in glioblastoma: effects on tumor progression and STAT3 signaling.Translational cancer research · 2026Article
- Atypical R-loops in cancer: decoding molecular chaos for therapeutic gain.Journal of translational medicine · 2025Review
- Aurora kinases signaling in cancer: from molecular perception to targeted therapies.Molecular cancer · 2025Review
- EHMT2-mediated R-loop formation promotes the malignant progression of prostate cancer via activating Aurora B.Clinical and translational medicine · 2025Article
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9 authors.
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Abstract
backgroundChromosomal instability (CIN), a hallmark of cancer, is commonly linked to poor prognosis in high-grade prostate cancer (PCa). Paradoxically, excessively high levels of CIN may impair cancer cell viability. Consequently, understanding how tumours adapt to CIN is critical for identifying novel therapeutic targets.
methodsBioinformatic analyses were conducted to identify genes overexpressed in PCa tissues using The Cancer Genome Atlas (TCGA) and GEO datasets. Western blotting and immunohistochemistry assays were applied to determine the expression levels of euchromatic histone lysine methyltransferase 2 (EHMT2), pT232-Aurora B and Cullin 3 (CUL3). The proliferation of cells was measured through CCK-8 tests, clonogenesis and subcutaneous xenografts of human PCa cells in BALB/c nude mice. Live cell imaging, immunofluorescence (IF) and flow cytometry were used to confirm the role of EHMT2 in PCa cell mitosis. Co-immunoprecipitation, Western blotting and IF assays further elucidated the underlying molecular mechanisms.
resultsEHMT2 was highly expressed in metastatic PCa tissues exhibiting elevated CIN and was strongly associated with adverse clinical outcomes in patients with PCa. Silencing EHMT2 impaired cell division, inducing G2/M-phase arrest and mitotic catastrophe in PCa cells. Mechanistically, EHMT2 is indispensable to ensure the full activation of Aurora B through centromeric R-loop-driven ATR-CHK1 pathway, with EHMT2 protein expression peaking during the G2/M-phase. Moreover, CUL3 was identified as a binding partner of EHMT2, mediating its polyubiquitination and destabilising its protein levels.
conclusionsThis study reveals a CUL3-EHMT2-Aurora B regulatory axis that safeguards accurate chromosome segregation in PCa cells, supporting the potential therapeutic application of EHMT2 inhibitors. KEY POINTS: Euchromatic histone lysine methyltransferase 2 (EHMT2) is overexpressed in advanced prostate cancer, restraining catastrophic chromosomal instability (CIN) and enhancing cell fitness. EHMT2 functions via the centromeric R-loop-driven ATR-CHK1-Aurora B pathway to promote chromosomal stability. EHMT2 confers enzalutamide resistance via activating Aurora B. Cullin 3 (CUL3) promotes EHMT2 destabilisation via deubiquitination.
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