A novel AGTPBP1-ERK/MYLK network mediates pancreatic cancer progression. (PubMed, Tissue Cell)
Mechanistically, AGTPBP1 activated the MAPK/ERK pathway through elevated ERK1/2 phosphorylation, and pharmacological inhibition of ERK phosphorylation using PD98059 abrogated both ERK phosphorylation and AGTPBP1-driven phenotypes, establishing ERK as an essential mediator...Notably, ERK signaling modulated MYLK activity (phosphorylated MYLK) without altering MYLK expression, indicating that AGTPBP1 regulates MYLK at the transcriptional level, whereas ERK controls its post-translational activity. Collectively, AGTPBP1 promotes PDAC progression through a dual mechanism involving ERK-dependent proliferative signaling and ERK-independent MYLK upregulation, positioning both molecules as potential therapeutic targets.