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Tight junction protein Junctional Adhesion Molecule-A regulates the expression of receptor tyrosine kinase EPHA2 in triple-negative breast cancer cells

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posted on 2022-08-03, 15:35 authored by Sri Harikrishna Vellanki, Viviana Bustos, Brian Harvey, Ann HopkinsAnn Hopkins

Breast tumors lacking expression of the human epidermal growth factor receptor-2 (HER2), progesterone receptor (PR) and estrogen receptor (ERα) are defined as triple negative breast cancers (TNBC). A lack of targeted therapies has impaired TNBC patient prognosis. It has previously been shown that high expression of Junctional Adhesion Molecule-A (JAM-A) correlates with aggressive breast cancer patient phenotypes, and that JAM-A regulates the expression of HER2 in breast cancer cells. Accordingly, we hypothesized that JAM-A might regulate the expression of other receptor tyrosine kinases. We show for the first time that JAM-A may regulate the expression of the EPHA2 receptor in TNBC cells and propose that this pathway merits deeper investigation for its therapeutic value in TNBC settings. 

Funding

Understanding the mechanistic role and druggability of JAM-A, an emerging upstream regulator of breast cancer tumourigenic signalling, using in vitro and in vivo methodologies and a novel small molecu | Funder: Science Foundation Ireland (SFI) | Grant ID: 13/IA/1994

Irish Government's Programme for Research in Third Level Institutions, Cycle 4, Ireland’s EU Structural Funds Programmes 2007-2013.

History

Comments

The original article is available at https://www.sciencerepository.org/

Published Citation

Vellanki SH, Bustos V, Harvey BJ, Hopkins AM. Tight junction protein junctional adhesion molecule-a regulates the expression of receptor tyrosine kinase EPHA2 in triple-negative breast cancer cells. Clin Oncol Res. 2019;2(4):1-4

Publication Date

10 August 2019

Department/Unit

  • Beaumont Hospital
  • Molecular Medicine
  • Surgery

Research Area

  • Cancer
  • Respiratory Medicine
  • Endocrinology

Publisher

Science Repository OU

Version

  • Published Version (Version of Record)