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<p>Lysine methyltransferase 5a (KMT5a) plays a key role in the pathogenesis of many human diseases. Here, we review the diverse impacts of KMT5a activity on human cancer development and progression. First, KMT5a is the only Mammalian enzyme that specifically induces monomethylation of histone 4 (H4) on lysine 20, thus regulating chromatin organization and, in turn, the transcription of several oncogenes and tumor suppressor genes. KMT5a, by inducing H4 methylation, also critically establishes the choice between different pathways of DNA double-strand break repair, with important consequences for genomic instability and cancer origin. Finally, KMT5a also methylates lysine residues on nonhistone proteins, and KMT5a-induced methylation of key oncogenic and tumor suppressor proteins, including TP53, strongly affects cancer cell functions. Overall, KMT5a is overexpressed in a high percentage and wide variety of human cancers and has protumorigenic activity, which makes it a target for innovative therapy.</p>

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Multiple functions of the lysine methyltransferase KMT5a in cancer: potential targets for innovative therapies

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月29日

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  • Rosa Della Monica,
  • Michela Buonaiuto,
  • Mariella Cuomo,
  • Davide Costabile,
  • Claudio Schonauer,
  • Giuseppe Catapano,
  • Lorenzo Chiariotti,
  • Roberta Visconti

摘要

Lysine methyltransferase 5a (KMT5a) plays a key role in the pathogenesis of many human diseases. Here, we review the diverse impacts of KMT5a activity on human cancer development and progression. First, KMT5a is the only Mammalian enzyme that specifically induces monomethylation of histone 4 (H4) on lysine 20, thus regulating chromatin organization and, in turn, the transcription of several oncogenes and tumor suppressor genes. KMT5a, by inducing H4 methylation, also critically establishes the choice between different pathways of DNA double-strand break repair, with important consequences for genomic instability and cancer origin. Finally, KMT5a also methylates lysine residues on nonhistone proteins, and KMT5a-induced methylation of key oncogenic and tumor suppressor proteins, including TP53, strongly affects cancer cell functions. Overall, KMT5a is overexpressed in a high percentage and wide variety of human cancers and has protumorigenic activity, which makes it a target for innovative therapy.