article = {COR-2019-4-101}
title = {Tight Junction Protein Junctional Adhesion Molecule-A Regulates the Expression of Receptor Tyrosine Kinase EPHA2 In Triple-Negative Breast Cancer Cells}
journal = {Clinical Oncology and Research}
year = {2019}
issn = {2613-4942}
doi = {http://dx.doi.org/10.31487/j.COR.2019.04.01}
url = {https://www.sciencerepository.org/tight-junction-protein-Jjunctional-adhesion-molecule-a-regulates-the-expression-of-receptor-tyrosine-kinase-epha2-in-triple-negative-breast-cancer-cells_COR-2019-4-101 
author = {Sri HariKrishna Vellanki,Viviana Bustos,Brian J. Harvey,Ann M. Hopkins,}
keywords = {Triple-negative breast cancer, tumor, tetrocarcin-A, JAM-A, EPHA2, ZO-1, cell viability, anti-tumor, tight junction}
abstract ={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.}