@article{Wang2023, 
author = {Feng Wang and Shitong Chen and Shihan Peng and Xujun Zhou and Houyi Tang and Hanghua Liang and Xi Zhong and He Yang and Xiaoxue Ke and MuHan Lü and Hongjuan Cui},
title = {PRMT1 promotes the proliferation and metastasis of gastric cancer cells by recruiting MLXIP for the transcriptional activation of the β-catenin pathway},
year = {2023},
journal = {Genes & Diseases},
volume = {10},
number = {6},
pages = {2622-2638},
keywords = {β-catenin signaling pathway, Gastric cancer, PRMT1, Transcriptional regulation, Ubiquitination},
url = {https://www.sciopen.com/article/10.1016/j.gendis.2023.02.006},
doi = {10.1016/j.gendis.2023.02.006},
abstract = {Protein arginine methyltransferase 1 (PRMT1), a type I PRMT, is overexpressed in gastric cancer (GC) cells. To elucidate the function of PRMT1 in GC, PRMT1 expression in HGC-27 and MKN-45 cells was knocked down by short hairpin RNA (shRNA) or inhibited by PRMT1 inhibitors (AMI-1 or DCLX069), which resulted in inhibition of GC cell proliferation, migration, invasion, and tumorigenesis in vitro and in vivo. MLX-interacting protein (MLXIP) and Kinectin 1 (KTN1) were identified as PRMT1-binding proteins. PRMT1 recruited MLXIP to the promoter of β-catenin, which induced β-catenin transcription and activated the β-catenin signaling pathway, promoting GC cell migration and metastasis. Furthermore, KTN1 inhibited the K48-linked ubiquitination of PRMT1 by decreasing the interaction between TRIM48 and PRMT1. Collectively, our findings reveal a mechanism by which PRMT1 promotes cell proliferation and metastasis mediated by the β-catenin signaling pathway.}
}