ArticleThe Kaohsiung journal of medical sciences2025
Mechanism of KDM5C-Mediated H3K4me3 Demethylation of HOXC-AS3 in the Proliferation of Colorectal Cancer Cells.
Article in The Kaohsiung journal of medical sciences, 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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Who cites it
2 citing papers in PubMed.
- The JMJD family histone demethylases: structure, mechanism of action, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- Mechanism of KDM5C-Mediated H3K4me3 Demethylation of HOXC-AS3 in the Proliferation of Colorectal Cancer Cells.The Kaohsiung journal of medical sciences · 2025Article
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4 authors.
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Abstract
Colorectal cancer (CRC) ranks as the third most prevalent malignancy and the second leading cause of cancer-related mortality worldwide. This study explored the role of lysine-specific histone demethylase 5C (KDM5C) in CRC progression. Expression levels of KDM5C, HOXC-AS3, and discs large MAGUK scaffold protein 4 (DLG4) were evaluated. Following the KDM5C knockdown, cell proliferation assays were conducted. The recruitment of KDM5C and histone H3 lysine 4 tri-methylation (H3K4me3) to the HOXC-AS3 promoter region was investigated. Furthermore, the subcellular distribution of HOXC-AS3 was assessed using nuclear-cytoplasmic fractionation and RNA fluorescence in situ hybridization (RNA-FISH). The interactions between HOXC-AS3, YTH domain-containing protein 1 (YTHDC1), and DLG4 were detected. The stability of DLG4 mRNA was evaluated, and the functional roles of HOXC-AS3 and DLG4 in CRC cells were examined through combined experimental analyses. KDM5C expression was elevated in CRC cells, whereas HOXC-AS3 and DLG4 levels were notably reduced. Silencing KDM5C resulted in suppressed cell proliferation. Mechanistically, KDM5C inhibited HOXC-AS3 expression by demethylating H3K4me3 at its promoter. HOXC-AS3 promoted DLG4 mRNA stability by recruiting the RNA-binding protein YTHDC1. Combined experimental results indicated that overexpression of HOXC-AS3 or DLG4 reduced the inhibitory effect of KDM5C downregulation on CRC cells. In conclusion, KDM5C promotes CRC cell proliferation by demethylating H3K4me3, repressing HOXC-AS3 expression. The reduced HOXC-AS3 levels impair the recruitment of YTHDC1, leading to decreased DLG4 expression.
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