BDNF/TrkB signaling protects HT-29 human colon cancer cells from EGFR inhibition.

摘要: The clinical success of targeted treatment colorectal cancer (CRC) is often limited by resistance to anti-epidermal growth factor receptor (EGFR) therapy. neurotrophin brain-derived neurotrophic (BDNF) and its TrkB have recently emerged as anticancer targets, we previously shown increased BDNF levels in CRC tumor samples. Here report the findings from vitro experiments suggesting that BDNF/TrkB signaling can protect cells antitumor effects EGFR blockade. anti-EGFR monoclonal antibody cetuximab reduced both cell proliferation mRNA expression human HT-29 cells. inhibitory effect on survival was counteracted addition recombinant BDNF. Finally, Trk inhibitor K252a synergistically enhanced proliferation, this blocked These results provide first evidence might play a role Moreover, it possible targeting could potentiate