LKB1 in lung cancerigenesis: a serine/threonine kinase as tumor suppressor.
10.1007/s13238-011-1021-6
- Author:
Yijun GAO
1
;
Gaoxiang GE
;
Hongbin JI
Author Information
1. Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
- Publication Type:Journal Article
- MeSH:
Carcinoma, Non-Small-Cell Lung;
enzymology;
metabolism;
Disease Progression;
Humans;
Lung Neoplasms;
enzymology;
metabolism;
Neoplasm Metastasis;
Protein-Serine-Threonine Kinases;
genetics;
metabolism;
physiology;
Signal Transduction;
Tumor Suppressor Proteins;
genetics;
metabolism
- From:
Protein & Cell
2011;2(2):99-107
- CountryChina
- Language:English
-
Abstract:
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.
