Downregulation of Bim by brain-derived neurotrophic factor activation of TrkB protects neuroblastoma cells from paclitaxel but not etoposide or cisplatin-induced cell death.

作者: Z Li , J Zhang , Z Liu , C-W Woo , C J Thiele

DOI: 10.1038/SJ.CDD.4401983

关键词:

摘要: Chemoresistance and increased expression of TrkB brain-derived neurotrophic factor (BDNF) are biomarkers poor prognosis in tumors from patients with neuroblastoma (NB). Previously, we found BDNF activation through PI3K/Akt protects NB etoposide/cisplatin-induced cell death. In this study, the role Bim, a proapoptotic protein, was investigated. Bim involved paclitaxel but not etoposide or cisplatin-induced death cells. Pharmacological genetic studies showed that BDNF-induced decreases were regulated by MAPK pathway. Both PI3K pathways protection cells paclitaxel-induced death, while predominantly mediated These data indicate different chemotherapeutic drugs induce distinct growth factors utilize signal transduction to modulate effects chemotherapy on

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