C-myc Contributes to Malignancy of Lung Cancer: A Potential Anticancer Drug Target

Emerging evidence has provided important information on oncoproteins involved in cancer initiation, progression, metastasis, and resistance to current therapies. C-myc, one of the critical oncoproteins, has been shown to be implicated in enhancing the aggressiveness of many cancers, mainly through its ability to increase cancer cell growth and cellular survival mechanisms. Despite the more precise and earlier detection and the availability of better therapies, lung cancer remains the most dreadful cancer as it causes high mortality rate with relatively poor treatment success. In lung cancer, C-myc is frequently dysregulated and associated with unfavorable patient survival. C-myc plays a role in regulation of lung cancer cell behaviors including growth, resistance, death, and dissemination through the activation of cell cycle driving proteins, an increase in the cellular levels of anti-apoptotic proteins, and the modulation of metabolism. Besides, C-myc has been shown to be important for cancer stem cell (CSC) properties. Taken together, targeting as well as inhibiting C-myc could provide promising means for resolving lung cancer. This review emphasizes on the molecular mechanism by which C-myc influences lung cancer growth, metastasis, drug resistance, and CSC maintenance, and suggests the target proteins that may benefit drug discovery and design.