SNORA33 promotes clear cell renal cell carcinoma development and resistance to sunitinib through triggering the JAK/STAT pathway

Accumulating evidence has confirmed that snoRNAs exert a role in a variety of cancer, however, less known in ccRCC. This study was aimed at elucidating the role and mechanism of snoRNAs in the tumorigenesis and progression of ccRCC. The snoRNAs expression matrices were obtained from the public TCGA and SNORic databases. The Kaplan-Meier analysis and Cox univariate and multivariate analyses confirmed the prognostic value of SNORA33 in ccRCC. A series of in vitro experiments were conducted to explore the functional role of SNORA33 in ccRCC. GSEA and western blot were used to explore and validate the involved mechanisms. SNORA33 was highly expressed in patients with ccRCC and was correlated with poor prognosis. The findings of in vitro experiments indicated that SNORA33 was capable of promoting the proliferation, invasion, migration, and resistance to sunitinib in ccRCC. SNORA33 is capable of attaining these effects through regulating the JAK/STAT signaling pathway.