POLM variant G312R promotes ovarian tumorigenesis through genomic instability and COL11A1-NF-κB axis

Abstract

Our research reveals that POLM plays an important role in ovarian cancer development, especially the mutation G312R. We uncover the POLM G312R mutation as a driver of genomic instability in ovarian cancer via aberrant ribonucleotide incorporation. We reveal that POLM G312R upregulates COL11A1 and activates NF-κB signaling, contributing to tumor progression and chemoresistance. This study identifies the POLM-COL11A1-NF-κB axis as a novel oncogenic pathway.