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AURKB and PI3K/AKT/mTOR pathways converge to regulate TERT expression.

Grace Lim1, Althea Bastian1,2, Saskia Fung1,3

  • 1Cancer Genetics Laboratory, Kolling Institute, Northern Clinical School, Faculty of Medicine and Health, The University of Sydney & Northern Sydney Local Health District, St Leonards, NSW, Australia.

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Summary

TERT promoter mutations drive cancer progression and can be targeted. New research reveals Aurora kinase B and TRIM28 regulate these mutations, offering potential therapeutic strategies for TERT promoter mutation-driven cancers.

Keywords:
Cell biologyMolecular biologyOncology

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Telomere length maintenance is crucial for cancer progression.
  • TERT promoter mutations (TERTp MUT) are poor prognostic markers and potential therapeutic targets due to their tumor specificity.

Purpose of the Study:

  • To identify novel pathways regulating TERT promoter mutation (TERTp MUT) activity.
  • To explore TERT promoter mutations as therapeutic targets in anaplastic thyroid cancer.

Main Methods:

  • CRISPR-Cas9 was used to generate SW1736 TERT/LUC cells with a luciferase reporter downstream of TERT promoter mutations.
  • A 218-kinase inhibitor library was screened to identify regulators of TERT promoter mutation activity.
  • Quantitative PCR, immunoprecipitation (IP), and chromatin IP were employed in thyroid cancer models.

Main Results:

  • PI3K/AKT/mTOR1 signaling and Aurora kinase B (AURKB) were identified as co-regulators of TERT promoter mutation activity, beyond MAPK signaling.
  • Distinct factors regulate wild-type and mutated TERT promoters.
  • AURKB, through REST, is recruited to TERT promoter mutations by TRIM28.

Conclusions:

  • TRIM28 is highlighted as a potential therapeutic target for cancers driven by TERT promoter mutations.
  • Understanding the distinct regulatory mechanisms of TERT promoters offers new avenues for cancer therapy.