Abstract
Background: As a key regulatory enzyme in mitochondria, YME1L is crucial for maintaining mitochondrial morphology, function and plasticity, and plays a
catalytic role in PDAC. The research team has found that the overexpression of YME1L can promote the expression of Gαi1 and the activation of Akt, and promote the progression of glioma. Taking NSCLC as the research material, this project aims to reveal the effect of YME1L regulating mitochondrial remodeling on the progress of NSCLC and its molecular mechanism, and provide new ideas for the treatment of NSCLC patients.
Results: YME1L is highly expressed in NSCLC tissues Overexpression of yme1l can promote Gαi1 expression and Akt activation, which in turn regulate cell proliferation, growth, migration and survival, and promote the progression of NSCLC.
Conclusions: In this study, we found that YME1L have a novel oncogenic role in promoting NSCLC tumorigenesis and progression via the Gαi1-AS-pAKT axis. The implementation of this project may provide a new entry point for the treatment of lung cancer.