LKB1/AMPK/mTOR Signaling Pathway in Non-small-cell Lung Cancer

被引:85
作者
Han, Dong [1 ]
Li, Shao-Jun [1 ]
Zhu, Yan-Ting [1 ]
Liu, Lu [1 ]
Li, Man-Xiang [1 ]
机构
[1] Xi An Jiao Tong Univ, Resp Dis Res Ctr, Dept Resp Med, Affiliated Hosp 2,Med Coll, Xian 710049, Peoples R China
关键词
LKB1; AMPK; mTOR; NSCLC; therapeutic target; ACTIVATED PROTEIN-KINASE; IONIZING-RADIATION; LKB1-AMPK PATHWAY; MAMMALIAN TARGET; MTOR; AMPK; GROWTH; LKB1; RAPAMYCIN; PHOSPHORYLATION;
D O I
10.7314/APJCP.2013.14.7.4033
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Links between cancer and metabolism have been suggested for a long time but compelling evidence for this hypothesis came from the recent molecular characterization of the LKB1/AMPK signaling pathway as a tumor suppressor axis. Besides the discovery of somatic mutations in the LKB1 gene in certain type of cancers, a critical emerging point was that the LKB1/AMPK axis remains generally functional and could be stimulated by pharmacological molecules such as metformin in cancer cells. In addition, AMPK plays a central role in the control of cell growth, proliferation and autophagy through the regulation of mTOR activity, which is consistently deregulated in cancer cells. Targeting of AMPK/mTOR is thus an attractive strategy in the development of therapeutic agents against non-small-cell lung cancer (NSCLC). In this review, the LKB1/AMPK/mTOR signaling pathway is described, highlighting its protective role, and opportunities for therapeutic intervention, and clinical trials in NSCLC.
引用
收藏
页码:4033 / 4039
页数:7
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