Abstract
Non-small cell lung cancer (NSCLC) represents around 80% of all lung cancer cases and is characterized by low survival rates, due to chemotherapy and radiation resistance. Novel treatment strategies for NSCLC are urgently needed. Liver kinase B1 (LKB1), a tumor suppressor commonly mutated in non-small cell lung cancer (NSCLC), activates AMP-activated protein kinase (AMPK) which in turn inhibits mammalian target of rapamycin complex 1 (mTORC1) and activates unc-51 like autophagy activating kinase 1 (ULK1) to promote autophagy.
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