Junctional adhesion molecule-A is co-expressed with HER2 in breast tumors and acts as a novel regulator of HER2 protein degradation and signaling

Dysregulation of junctional adhesion molecule-A via p63/GATA-3 in head and neck squamous cell carcinoma

“…JAM-A stabiles HER2 expression in breast cancer via PI3K and MAPK pathways, which results in cell proliferation [14]. Furthermore, JAM-A regulates epithelial proliferation through Akt/β-catenin signalling in intestinal epithelial cell proliferation in a dimerization-dependent manner [15].…”

“…JAM-A stabiles HER2 expression in breast cancer via PI3K and MAPK pathways, which results in cell proliferation [14]. It also contributes to intestinal epithelial homeostasis by regulating an Akt/β-catenin signalling pathway [15].…”

Neutrophil-Epithelial Interactions

“…66,108 Indeed, altered disease progression observed in certain types of cancer has also been linked to cellular levels of JAM-A and b1 integrin. 109,110 Signaling pathways downstream of JAM-A that regulate barrier, migration, and proliferation are summarized in Figure 5B.…”

The Contribution of Ig-Superfamily and MARVEL D Tight Junction Proteins to Cancer Pathobiology

“…Overexpression of JAM-A has been linked with increased risk of metastasis in several independent cohorts of breast cancer patients (14)(15)(16). Mechanistically, growth impairment of JAM-A-deficient tumors has been demonstrated in a mammary gland-specific polyoma virus middle T-antigen (MMTV-PyVmT) mouse model of breast cancer, while abrogation of JAM-A expression in breast cancer cells has been linked with the induction of apoptosis and with reduced breast cancer progression (16).…”

“…Mechanistically, growth impairment of JAM-A-deficient tumors has been demonstrated in a mammary gland-specific polyoma virus middle T-antigen (MMTV-PyVmT) mouse model of breast cancer, while abrogation of JAM-A expression in breast cancer cells has been linked with the induction of apoptosis and with reduced breast cancer progression (16). Further evidence implicating JAM-A in breast cancer cell survival signaling has accrued from a study in which it was described as a novel regulator of HER2 protein degradation and signaling (15). In terms of the therapeutic potential of targeting JAM-A, its pharmacological inhibition using a monoclonal antibody has been demonstrated to significantly inhibit tumor growth in murine xenograft models of human tumors (17).…”