Autophagy-related signaling pathways in non-small cell lung cancer

Lung cancer is one of the most prevalent causes of morbidity and mortality in both men and women across the globe. The disease has a quiet phenotype at first, which leads to chronic tumor development. Non-small cell lung cancer (NSCLC) is the most common kind of lung cancer, accounting for 85 percent of all lung malignancies. Autophagy has been described as an intracellular “recycle bin” where damaged proteins and molecules are degraded. Autophagy regulation is mainly dependent on signaling pathways such as phosphoinositide 3-kinases (PI3K), AKT, and the mammalian target of rapamycin (mTOR). In the context of NSCLC, studies on these signaling pathways are inconsistent, but our literature review suggests that the inhibition of mTOR, PI3K/AKT, and epidermal growth factor receptor signaling pathways by different medications can active autophagy and inhibit NSCLC progression. In conclusion, signaling pathways related to autophagy are effective therapeutic approaches for the treatment of NSCLC.