Related Experiment Video

Updated: Jun 9, 2025

Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors
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Histone-Lysine N-Methyltransferase 2D (KMT2D) Impending Therapeutic Target for the Management of Cancer: The Giant

Meshak Dhanashekaran Cecileya Jasmin1, Narayanaswamy Radhakrishnan2, Venugopal Vinod Prabhu3

  • 1Department of Biochemistry, Saveetha Medical College and Hospital, Saveetha Institute of Medical and Technical Sciences (Deemed to be University), Thandalam, Chennai, Tamil Nadu 602105, India; Department of Biochemistry, Tagore Medical College and Hospital, Rathinamangalam, Melakottaiyur, Chennai, Tamil Nadu 600127, India.

Journal of Environmental Pathology, Toxicology and Oncology : Official Organ of the International Society for Environmental Toxicology and Cancer
|October 27, 2024
PubMed

Insights

The histone-lysine N-methyltransferase 2D (KMT2D) gene, a tumor suppressor, is crucial in cancer development. Targeting KMT2D may offer new therapies by downregulating genes that drive aggressive tumor progression.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Histone-lysine N-methyltransferase 2D (KMT2D) is a tumor suppressor and key regulator of histone methylation.
  • KMT2D mutations are linked to various cancers, including lymphoma, medulloblastoma, and lung carcinoma.
  • Epigenetic alterations in KMT2D influence cancer initiation, progression, and cell migration.

Purpose of the Study:

  • To review recent research on the KMT2D gene's role in oncogenesis.
  • To highlight KMT2D as a potential therapeutic target for cancer management.
  • To explore KMT2D's function in regulating gene expression for cancer inhibition.

Main Methods:

  • Literature review of recent research on KMT2D.
  • Analysis of KMT2D's role in epigenetic alterations and gene regulation.
  • Identification of downstream targets regulated by KMT2D.

Main Results:

  • KMT2D deficiency promotes cancer development and cell migration.
  • Loss of KMT2D activates glycolytic genes, driving aggressive tumor progression.
  • KMT2D regulates key pathways including EGFR-TK, RTK-RAS signaling, and RAS activator genes.

Conclusions:

  • KMT2D is a critical factor in cancer pathogenesis.
  • Targeting KMT2D could lead to novel therapeutic strategies for downregulating oncogenic genes.
  • Understanding KMT2D gene expression is vital for developing targeted cancer therapies.

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