Abstract
Breast tumors lacking expression of the human epidermal growth factor receptor-2 (HER2), progesterone receptor (PR) and estrogen receptor (ER?) 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.
Highlights
Tumors lacking the expression of human epidermal growth factor receptor-2 (HER2), progesterone receptor (PR) and ERα are defined as triple negative breast cancers (TNBC)
Since Junctional Adhesion MoleculeA (JAM-A) expression has been shown to regulate the expression of HER2 in breast cancer cells, in this manuscript we sought to uncover if JAM-A regulates the expression of other receptor tyrosine kinases relevant to TNBC settings [4]
Since JAM-A regulates the expression of the receptor tyrosine kinase HER2 in breast cancer cells, we hypothesized that JAM-A might regulate other receptor tyrosine kinases relevant to TNBC settings [4]
Summary
Tumors lacking the expression of HER2, PR and ERα are defined as triple negative breast cancers (TNBC). Due to a lack of targeted therapies the standard of care for treating TNBC patients during early and advanced stage of the disease is chemotherapy [1]. TNBC patients frequently develop resistance to chemotherapeutic drugs relatively quickly, leading to an early demise. The lack of targeted therapies and poor prognosis of patients with TNBC have fostered a major effort to discover actionable molecular targets to treat patients with these tumours [1]. In the present study we extend prior work proposing that the tight junction protein Junctional Adhesion MoleculeA (JAM-A) is a potential therapeutic target in TNBC settings. High JAM-A high expression has previously been correlated with aggressive disease and poor outcome in breast cancer patients [2, 3]. We have shown that JAM-A regulates the expression of the receptor tyrosine kinase HER2 in breast cancer cells [4]
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