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.
CITATION STYLE
Han, D., Li, S. J., Zhu, Y. T., Liu, L., & Li, M. X. (2013). LKB1/AMPK/mTOR Signaling Pathway in Non-small-cell Lung Cancer. Asian Pacific Journal of Cancer Prevention. Asian Pacific Organization for Cancer Prevention. https://doi.org/10.7314/APJCP.2013.14.7.4033
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