2. Academic Validation
  3. Methylation of HBP1 by PRMT1 promotes tumor progression by regulating actin cytoskeleton remodeling

Methylation of HBP1 by PRMT1 promotes tumor progression by regulating actin cytoskeleton remodeling

  • Oncogenesis. 2022 Aug 8;11(1):45. doi: 10.1038/s41389-022-00421-7.
Jiyin Wang 1,  Ruixiang Yang 1,  Yuning Cheng 1,  Yue Zhou 1,  Tongjia Zhang 1,  Shujie Wang 1,  Hui Li 1,  Wei Jiang 1,  Xiaowei Zhang 2
Affiliations

Affiliations

  • 1 Department of Biochemistry and Biophysics, School of Basic Medical Sciences, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Peking University Health Science Center, Beijing, 100191, P. R. China.
  • 2 Department of Biochemistry and Biophysics, School of Basic Medical Sciences, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Peking University Health Science Center, Beijing, 100191, P. R. China. xiaoweizhang@bjmu.edu.cn.
PMID: 35941115 DOI: 10.1038/s41389-022-00421-7
Abstract

HBP1 is a sequence-specific transcription factor which generally considered as a crucial growth inhibitor. Posttranslational modification of HBP1 is vital for its function. In this study, we demonstrate that HBP1 is methylated at R378 by PRMT1, which decreases HBP1 protein stability by promoting its ubiquitination and proteasome-mediated degradation. PRMT1-mediated methylation of HBP1 alleviates the repressive effects of HBP1 on tumor metastasis and growth. GSN is identified as a novel target gene of HBP1. Methylation of HBP1 promotes actin Cytoskeleton remodeling, glycolysis and tumor progression by downregulating GSN (a vital actin-binding protein) levels. The methylated HBP1-GSN axis is associated with the clinical outcomes of Cancer patients. This investigation elucidates the mechanism of how methylated HBP1 facilitates actin Cytoskeleton remodeling, thus attenuates its tumor-suppressive function and promotes tumor progression. Targeting methylated HBP1-GSN axis may provide a therapeutic strategy for Cancer.

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