Targeting ACE2-BRD4 crosstalk in colorectal cancer and the deregulation of DNA repair and apoptosis

  • NPJ Precis Oncol. 2023 Feb 18;7(1):20. doi: 10.1038/s41698-023-00361-4.
Shilan Zhang  1 ,  Sabeeta Kapoor  1 ,  Chakrapani Tripathi  1 ,  Jorge Tovar Perez  1 ,  Nivedhitha Mohan  1 ,  Wan Mohaiza Dashwood  1 ,  Ke Zhang  1 ,  Praveen Rajendran  2 ,  Roderick Dashwood  3  4
Affiliations
  • 1. Center for Epigenetics & Disease Prevention, Texas A&M Health, and Department of Translational Medical Sciences, Texas A&M School of Medicine, Houston, TX, USA.
  • 2. Center for Epigenetics & Disease Prevention, Texas A&M Health, and Department of Translational Medical Sciences, Texas A&M School of Medicine, Houston, TX, USA. [email protected].
  • 3. Center for Epigenetics & Disease Prevention, Texas A&M Health, and Department of Translational Medical Sciences, Texas A&M School of Medicine, Houston, TX, USA. [email protected].
  • 4. Department of Clinical Cancer Prevention, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. [email protected].
PMID: 36801948 DOI: 10.1038/s41698-023-00361-4
Abstract

ACE2 overexpression in colorectal Cancer patients might increase susceptibility to SARS-CoV-2 Infection. We report that knockdown, forced overexpression, and pharmacologic inhibition in human colon Cancer cells targeted ACE2-BRD4 crosstalk to mediate marked changes in DNA damage/repair and Apoptosis. In colorectal Cancer patients for whom high ACE2 plus high BRD4 expression is predictive of poor survival, pan-BET inhibition would need to consider proviral/Antiviral actions of different BET proteins during SARS-CoV-2 Infection.

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