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Publication : TRAF1 Is Critical for Regulating the BRAF/MEK/ERK Pathway in Non-Small Cell Lung Carcinogenesis.

First Author  Wang Q Year  2018
Journal  Cancer Res Volume  78
Issue  14 Pages  3982-3994
PubMed ID  29748372 Mgi Jnum  J:264288
Mgi Id  MGI:6195919 Doi  10.1158/0008-5472.CAN-18-0429
Citation  Wang Q, et al. (2018) TRAF1 Is Critical for Regulating the BRAF/MEK/ERK Pathway in Non-Small Cell Lung Carcinogenesis. Cancer Res 78(14):3982-3994
abstractText  Tumor necrosis factor receptor (TNFR)-associated factor 1 (TRAF1) is a unique TRAF protein that can interact directly or indirectly with multiple TNFR family members, regulatory proteins, kinases, and adaptors that contribute to its diverse functions in specific tissues. However, the role of TRAF1 in non-small cell lung cancer (NSCLC) remains unknown. In this study, we report that TRAF1 is overexpressed in human lung cancer cells and tissues. TRAF1 expression level inversely correlated with patient survival probability. Loss of TRAF1 decelerated tumor invasion in a urethane-induced lung carcinogenesis mouse model. Furthermore, TRAF1 expression affected TRAF2-mediated BRAF Lys48-linked ubiquitination, which was followed by the inhibition of growth and differentiation, and the induction of death in lung cancer cells. Overall, our work suggests that TRAF1 plays a novel role in the regulation of the BRAF/MEK/ERK signaling pathway in NSCLC and offers a candidate molecular target for lung cancer prevention and therapy.Significance: These findings identify TRAF1 as a new therapeutic target for NSCLC. Cancer Res; 78(14); 3982-94. (c)2018 AACR.
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