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Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors
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A human tRNA methyltransferase 9-like protein prevents tumour growth by regulating LIN9 and HIF1-α

Ulrike Begley1, Maria Soledad Sosa, Alvaro Avivar-Valderas

  • 1College of Nanoscale Science and Engineering, University at Albany, State University of New York, Albany, NY, USA.

EMBO Molecular Medicine
|February 6, 2013
PubMed

Insights

The tRNA methyltransferase 9-like (hTRM9L) enzyme suppresses tumor growth by regulating cell proliferation and response to hypoxia. hTRM9L deficiency increases sensitivity to aminoglycoside antibiotics in cancer treatment.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Biochemistry

Background:

  • Aberrant translation regulation drives cancer cell transformation.
  • tRNA modifications directly control translation, suggesting tRNA modifying enzymes regulate cancer progression.

Purpose of the Study:

  • Investigate the role of tRNA methyltransferase 9-like (hTRM9L) in cancer progression.
  • Determine the therapeutic potential of targeting hTRM9L or its associated pathways.

Main Methods:

  • Analysis of hTRM9L mRNA levels in various carcinomas.
  • In vivo tumor growth suppression assays in colon carcinoma cell lines (SW620, HCT116) with re-expressed hTRM9L.
  • Assessment of proliferation, cell cycle arrest, LIN9 expression, HIF1-α/GLUT1 pathway, and response to aminoglycoside antibiotics.

Main Results:

  • hTRM9L mRNA is down-regulated in multiple cancer types.
  • hTRM9L re-expression suppressed tumor growth, decreased proliferation, induced G0/G1 arrest, and upregulated LIN9.
  • hTRM9L re-expression inhibited hypoxia-induced GLUT1 expression via HIF1-α.
  • hTRM9L-deficient tumors showed increased sensitivity to aminoglycoside antibiotics.

Conclusions:

  • hTRM9L and tRNA modifications inhibit tumor growth through LIN9 and HIF1-α-dependent mechanisms.
  • Aminoglycoside antibiotics may be effective for treating hTRM9L-deficient tumors.

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