ELK1/NOL3/GRP78 axis regulates proliferation and stemness in TP53-mutant colon cancer by enhancing adaptive endoplasmic reticulum stress - PubMed
6 hours ago
- #cancer stemness
- #ER stress
- #colon cancer
- The ELK1/NOL3/GRP78 axis regulates proliferation and stemness in TP53-mutant colon cancer by enhancing adaptive endoplasmic reticulum (ER) stress.
- TP53-mutant colon cancer is aggressive and linked to poor survival, with adaptive ER stress promoting metabolic plasticity and chemoresistance.
- Single-cell RNA-seq identified ER stress- and mitochondrial metabolism-related genes (EMRDEGs) in TP53-mutant vs. wild-type tumors.
- NOL3 was identified as an independent adverse prognostic factor, correlating with advanced stage, nodal positivity, and shorter survival.
- NOL3 enhances proliferation and stemness in TP53-mutant colon cancer cells by interacting with GRP78 to activate the PERK/CHOP pathway.
- ELK1 transcriptionally upregulates NOL3, forming a key regulatory axis in TP53-mutant colon cancer progression.
- NOL3 serves as a potential prognostic biomarker and therapeutic target for TP53-mutant colon cancer.