Translated Abstract
Lung cancer, as the most common malignant tumour, have increased significantly every year. In our country, the incidence of lung cancer has become the highest among cancer. About 85% of the annual new cases is non-small cell lung cancer(NSCLC). Although much progress has been made in the diagnosis and treatment of NSCLC, the five-years survival rate remains low. Therefore, it is important to explor the possible molecular mechanism of pathogenesis for the diagnosis and treatment of NSCLC. LKB1, a cancer suppressor gene which regulated multiple cell signal transduction, is involved in the energy metabolism and the cell polarity. AMPK/mTOR is an improtant drownstream signal pathway of LKB1. AMPK, a energy sensor of cell, is regulated by the level of cell energy, can respound to the change of AMP/ATP ratio and maintain the energy homeostasis. The activity of mTOR can inhibit autophagy. LKB1 can positive regulate autophagy through the activition of AMPK-induced inhibiton of mTOR. The somatic mutation of LKB1 is a common event in NSCLC. A part of mutations leads to truncations of LKB1 protein. In our previous research, we found that LKB1 can suppresse the proliferation, migration and invasion in lung adenocacinoma cell lines H1299 and H1975, and can regulate autophagy through the interaction with SESN2. However, it still remains unclear of the function of LKB1 turncation protein. Hence, illuminating the role of LKB1 truncation will countribute to make further understanding of LKB1 in lung cancer, which can provide a new clue in the treatment of NSCLC.
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