PRMT6 acts as a pro-angiogenic factor in colorectal cancer.

Authors

Haifeng Han, Xin Zhang, Mingxin Jin, Yali Chu, Fengjun Liu, Hui Qu, Cheng Chen

Published in

Cell death discovery. Jul 11, 2026. Epub Jul 11, 2026.

Abstract

The progression of colorectal cancer (CRC) is highly dependent on tumor angiogenesis, a process primarily regulated by hypoxia-inducible factor HIF-1α. This study focuses on the mechanistic role of protein arginine methyltransferase 6 (PRMT6) in CRC angiogenesis and reveals that PRMT6 is significantly overexpressed in CRC tissues, stabilizing HIF-1α via the autophagy-lysosome pathway. Specifically, PRMT6 catalyzes the asymmetric dimethylation of HIF-1α at arginine 463, which disrupts its interaction with the autophagy-related protein TAX1BP1, thereby preventing its degradation. In vivo experiments demonstrate that PRMT6 silencing reduces HIF-1α stability, decreases vascular endothelial growth factor A (VEGFA) expression, and markedly suppresses tumor angiogenesis and growth. This study identifies the PRMT6-HIF-1α axis as a novel therapeutic target for CRC and suggests that targeting this pathway may facilitate the development of precision anti-angiogenic therapies.

PMID:
42436163
Bibliographic data and abstract were imported from PubMed on 12 Jul 2026.

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