BMX kinase (also termed ETK) is a member of the TEC family of non-receptor tyrosine kinases (which also includes ITK, TEC, BTK and TXK), and is the major member of this family expressed in epithelial cells, including prostate epithelium. Similar to the SRC family of kinases, the TEC kinases contain core SH3, SH2 and kinase domains, binds to membrane-associated PIPs in a manner similar to Akt.
BMX is further activated by the subsequent phosphorylation of a tyrosine in its kinase domain by membrane-associated SRC. The activation of BMX in response to PI-3K signaling, which is increased in prostate cancer (PCa) due to PTEN loss, suggests a potential role for BMX in PCa. Indeed, BMX expression is increased in PCa, and transgenic over-expression of BMX in mouse prostate epithelium causes hyperplasia and contributes to development of dysplastic lesions resembling human prostate intraepithelial neoplasia (PIN). The irreversible BMX kinase inhibitor, BMX-IN-1, demonstrates antiproliferation efficacy against prostate cancer cells.
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