Commentary Open Access
Volume 1 | Issue 4 | DOI: https://doi.org/10.33696/Signaling.1.030

PRMT1-catalyzed SMAD7 Arginine Methylation Bridges EMT and Stemness

  • 1Central laboratory, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei, China
  • 2Center for Craniofacial Molecular Biology, Herman Ostrow School of Dentistry, University of Southern California, Los Angeles,CA, USA
  • 3Biochemistry and Molecular Medicine, University of Southern California, Los Angeles, CA, USA
  • 4Norris Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA
+ Affiliations - Affiliations

Corresponding Author

Jian Xu, xujian@usc.edu

Received Date: September 08, 2020

Accepted Date: November 06, 2020


Epithelial-mesenchymal transition (EMT), a lineage transition from epithelium to mesenchyme, is induced by a convergence of signaling pathways and often driven by TGFß/SMAD signaling. Except for its critical roles on cell shape and motility during cancer invasion and metastasis, TGFß/SMAD activation-induced EMT has also been reported to be involved in cancer stem cell (CSC) generation. We studied the role of PRMT1 in TGFß/SMAD signaling and found that PRMT1-catalyzed arginine methylation of SMAD7 is required for TGFß/SMAD signaling, and thus critical for TGFß-induced EMT and maintenance of epithelial stemness. Together with the emerging associations between SMAD7, EMT and the sustenance of CSC, PRMT1-catalyzed SMAD7 arginine methylation is not only required for TGFß/SMAD signaling, more importantly, it also bridges EMT and stemness. Here, we offer perspectives on PRMT1 and SMAD7 methylation as potential therapeutic targets for tumor dissemination and relapse.


Arginine methylation, PRMT1, SMAD7, TGFβ, EMT, Stemness

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