TMEM44 as a Novel Prognostic Marker for Kidney Renal Clear Cell Carcinoma is Associated with Tumor Invasion, Migration and Immune Infiltration.

Transmembrane (TMEM) proteins are integral membrane proteins that traverse biological membranes. Several members of the TMEM family have been linked to the development and progression of various tumors. However, the specific role and mechanism of TMEM44 in tumor biology remain largely unexplored. In this study, we initially conducted an extensive analysis using the TCGA database to investigate the expression patterns and survival associations of TMEM44 across various human tumors. Subsequently, we focused on KIRC and found a significant correlation between TMEM44 expression and this particular cancer type. To validate our findings, we performed western blot and quantitative polymerase chain reaction (qPCR) assays to confirm the expression levels of TMEM44 in KIRC. Following this, we employed a series of functional assays, including CCK8 viability assay, EDU incorporation assay, wound healing assay, and transwell migration assay, to investigate the biological role of TMEM44 in KIRC. We observed a significant upregulation of TMEM44 expression in KIRC, indicating its potential involvement in the pathogenesis of this cancer. We intervened in the expression of TMEM44 in KIRC cells and found significant inhibitory effects on cell proliferation, migration, and invasion in KIRC cells. Furthermore, our findings indicated that TMEM44 could serve as an independent prognostic factor in KIRC, highlighting its potential clinical significance. Consequently, TMEM44 holds promise as both a prognostic biomarker and a prospective therapeutic target for KIRC.

PRMT7 promotes the growth of renal cell carcinoma through modulating the ß-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 ß-catenin and inhibiting the ubiquitin-mediated degradation of ß-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 ß-catenin/C-MYC axis, thereby providing new strategies and targets for the treatment of ccRCC patients.