PRMT7 promotes the growth of renal cell carcinoma through modulating the β-catenin/C-MYC axis.

Arginine methylation is mainly catalyzed by protein arginine methyltransferases (PRMTs) and is one of the most common posttranslational modifications closely related to the development of cancer. PRMT7 is overexpressed in various tumors and promotes the malignant progression of tumors, but the expression and role of PRMT7 in renal cell carcinoma (RCC) remains unclear. Here, we report for the first time that the expression of PRMT7 is increased in clear cell renal cell carcinoma (ccRCC) tissues and that it may act as an independent predictor for the poor prognosis of ccRCC patients. We found that PRMT7 promotes RCC cell proliferation both in vitro and in vivo. Moreover, the methyltransferase inhibitor adenosine dialdehyde (Adox) blocks the action of PRMT7 in ccRCC cells. Furthermore, PRMT7 regulates the expression of C-MYC, which plays an important role in promoting ccRCC cell proliferation, and it accelerates the tumor development of RCC in a C-MYC-dependent manner. Mechanistically, PRMT7 upregulates the expression of C-MYC via methylating β-catenin and inhibiting the ubiquitin-mediated degradation of β-catenin. In conclusion, our study demonstrates that overexpressed PRMT7 in ccRCC cells acts as an oncogene to promote the growth of renal cell carcinoma through regulating the β-catenin/C-MYC axis, thereby providing new strategies and targets for the treatment of ccRCC patients.