黑色素瘤
MAPK/ERK通路
癌症研究
MEK抑制剂
突变体
转移
生物
细胞外信号调节激酶
癌症
信号转导
医学
细胞生物学
内科学
遗传学
基因
作者
Berta Sanchez‐Laorden,Amaya Virós,María Romina Girotti,Malin Pedersen,Grazia Saturno,Alfonso Zambon,Dan Niculescu‐Duvaz,Samra Turajlic,Andrew Hayes,Martin Gore,James Larkin,Paul Lorigan,Martin Cook,Caroline J. Springer,Richard Marais
出处
期刊:Science Signaling
[American Association for the Advancement of Science]
日期:2014-03-25
卷期号:7 (318): ra30-ra30
被引量:127
标识
DOI:10.1126/scisignal.2004815
摘要
Melanoma is a highly metastatic and lethal form of skin cancer. The protein kinase BRAF is mutated in about 40% of melanomas, and BRAF inhibitors improve progression-free and overall survival in these patients. However, after a relatively short period of disease control, most patients develop resistance because of reactivation of the RAF-ERK (extracellular signal-regulated kinase) pathway, mediated in many cases by mutations in RAS. We found that BRAF inhibition induces invasion and metastasis in RAS mutant melanoma cells through a mechanism mediated by the reactivation of the MEK (mitogen-activated protein kinase kinase)-ERK pathway, increased expression and secretion of interleukin 8, and induction of protease-dependent invasion. These events were accompanied by a cell morphology switch from predominantly rounded to predominantly elongated cells. We also observed similar responses in BRAF inhibitor-resistant melanoma cells. These data show that BRAF inhibitors can induce melanoma cell invasion and metastasis in tumors that develop resistance to these drugs.
科研通智能强力驱动
Strongly Powered by AbleSci AI