Tricin selectively combats KRAS-mutant non-small cell lung cancer by inhibiting the PDGF-BB-induced SRC/MAPK/AP-1/PD-L1 signaling pathway and potentiating the antitumor effect of an anti-PD-1 antibody.

ABSTRACT:

Background

KRAS is a commonly mutated gene that is present in approximately 30% of NSCLC patients. Currently, the identification of effective therapies for KRAS-mutant NSCLC is difficult for reasons of the structural and biochemical characteristics of the KRAS protein. Our previous study has revealed that tricin was a bioactive component having selective effects on KRAS^G12C-mutant NSCLC cell lines. Thus, our aim in this project was to explore the mechanism by which tricin inhibited the progression of KRAS-mutant NSCLC much more deeply.

Methods

First of all, we detected the acute toxicity of an intraperitoneal injection of tricin in mice according to the improved up-and-down procedure. Next, we integrated network pharmacology, molecular docking with transcriptomics

SUBMITTER: Li JX 

PROVIDER: S-EPMC12209307 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature