Loss-of-function mutations in KEAP1 drive lung cancer progression via KEAP1/NRF2 pathway activation.

ABSTRACT:

Background and purpose

Targeted therapy and immunotherapy have led to dramatic change in the treatment of lung cancer, however, the overall 5-year survival rate of lung cancer patients is still suboptimal. It is important to exploit new potential of molecularly targeted therapies. High-frequency somatic mutations in KEAP1/NRF2 (27.9%) have been identified in lung squamous cell carcinoma. In this research, we explored the role of KEAP1 somatic mutations in the development of LSCC and whether a nuclear factor erythroid 2-related factor 2(NRF2) inhibitor be potential to target lung cancer carrying KEAP1/NRF2 mutations.

Methods

Lung cancer cell lines A549 and H460 with loss-of-function mutations in KEAP1 stably transfected with wild-type (WT) KEAP1 or somatic mutations in KEAP1

SUBMITTER: Gong M 

PROVIDER: S-EPMC7310414 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature