Abstract
Patients with polycystic kidney disease (PKD) have a high risk of developing renal cell carcinoma (RCC). SET domain–containing 2(SETD2) is the only molecule known to regulate lysine trimethylation (H3K3me3) of histone H3 in human tissue, and SETD2 is identified as a tumor suppressor in ccRCC. Although there are some studies revealing some mechanism about PKD developing ccRCC, the underlying mechanism remains largely reported. We collected the Kidney samples from SETD2 conditional knockout mice described before (Rao, 2021) and detected the expression levels of some important genes related to Akt/mTOR signaling pathway. Besides, we found that SETD2 is closely related to Akt/mTOR signaling pathway and can be regulated by Western blot analysis, qRT-PCR and immunofluorescence. For clinical translation, the cross-talks between SETD2 and Akt/mTOR signaling may provide a potential strategy to prevent tumorigenesis in patients with ccRCC therapy.