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.

精氨酸甲基化主要由蛋白质精氨酸甲基转移酶（PRMT）催化，是与癌症的发展密切相关的最常见的翻译后修饰之一。PRMT7在各种肿瘤中过表达并促进肿瘤的恶性进展，但PRMT7在肾细胞癌（RCC）中的表达和作用尚不清楚。在这里，我们首次报告在透明细胞肾细胞癌（ccRCC）组织中PRMT7的表达增加，并且它可以作为ccRCC患者预后不良的独立预测因子。我们发现PRMT7在体外和体内均可促进RCC细胞增殖。此外，甲基转移酶抑制剂腺苷二醛（Adox）阻断了PRRC7在ccRCC细胞中的作用。此外，PRMT7调节C-MYC的表达，这在促进ccRCC细胞增殖中起重要作用，并以C-MYC依赖性方式促进RCC的肿瘤发展。从机理上讲，PRMT7通过使β-catenin甲基化并抑制泛素介导的β-catenin降解来上调C-MYC的表达。总之，我们的研究表明，ccRCC细胞中过表达的PRMT7作为致癌基因，通过调节β-catenin/ C-MYC轴来促进肾癌的生长，从而为ccRCC患者的治疗提供了新的策略和目标。