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作 者:Yijun Gao Gaoxiang Ge Hongbin Ji
机构地区:[1]Laboratory of Molecular Cell Biology,Institute of Biochemistry and Cell Biology,Shanghai Institutes for Biological Sciences,Chinese Academy of Sciences,Shanghai 200031,China [2]State Key Laboratory of Molecular Biology,Institute of Biochemistry and Cell Biology,Shanghai Institutes for Biological Sciences,Chinese Academy of Sciences,Shanghai 200031,China
出 处:《Protein & Cell》2011年第2期99-107,共9页蛋白质与细胞(英文版)
基 金:the National Basic Research Program of China(Grant No.2010CB912102);the National Natural Science Foundation of China(Grant Nos.30871284,30971461 and 30971495);the Science and Technology Commission of Shanghai Municipality(No.09JC1416300)。
摘 要:Lung cancer is featured with high mortality,with a 15%five-year survival rate worldwide.Genetic alterations,such as loss of function of tumor suppressor genes,frequently contribute to lung cancer initiation,progression and metastasis.Liver kinase B1(LKB1),as a serine/threonine kinase and tumor suppressor,is frequently mutated and inactivated in non-small cell lung cancer(NSCLC).Recent studies have provided strong evidences that LKB1 loss promotes lung cancerigenesis process,especially lung cancer progression and metastasis.This review will summarize recent progress on how LKB1 modulates the process of lung cancerigenesis,emphasizing on LKB1 downstream signaling pathways and biological functions.We will further discuss the potential development of prognostic biomarkers or therapeutic targets in lung cancer clinic based on the molecular alteration associated with deregulated LKB1 signaling.
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