Author(s)

Yu Wang

Corresponding Author

Yu Wang

ABSTRACT

Metabolic reprogramming affects the development and metastasis of non-small cell lung cancer (NSCLC), in which oxidative stress, endoplasmic reticulum stress, and epigenetic modification all play key roles. From these aspects, the mechanism of metabolic reprogramming in non-small cell lung cancer was analyzed. The key regulatory protein in oxidative stress is NRF2, which has multifaceted effects on lung cancer, RRBP1 protein plays an important role in endoplasmic reticulum stress, that is vital in tumor survival as well as endoplasmic reticulum stress. Autophagy may be activated through the AMPK-mTOR pathway. These findings provide important directions for subsequent tumor therapy. Cancer-associated fibroblasts play an important role in the epigenetic modification of non-small cell lung cancer, which also explains that the annexin A6 molecule secreted by CAFs can lead to the resistance of anticancer drugs. T cells (including CD4+ T cells, CD8+ T cells, and regulatory T cells) play an important role in the epigenetic regulation of tumor cells. Therefore, future NSCLC treatment will focus on resistance in immunotherapy and targeted therapy problem, from which T cell therapy will provide more directions. More importantly, combination therapy has become an important direction to solve metabolic reprogramming.

KEYWORDS

Non-small cell lung cancer, ROS, ER stress, epigenetic, TME