Risk signature identification and NPRL2 affects sunitinib sensitivity in clear cell renal cell carcinoma

肾透明细胞癌 舒尼替尼 癌症研究 癌变 生物 细胞生长 细胞 细胞周期 PI3K/AKT/mTOR通路 抑癌基因 细胞凋亡 癌症 肾细胞癌 内科学 医学 遗传学
作者
Xiaoyi Du,Zhipeng Zhao,Xin Zhao,Hexi Wang,Li Jiang,Wei Tang
出处
期刊:Biochemical and Biophysical Research Communications [Elsevier]
卷期号:663: 122-131
标识
DOI:10.1016/j.bbrc.2023.04.063
摘要

Tumor suppressor genes (TSGs) play a crucial role in tumorigenesis and drug resistance. We analyzed the subtypes of clear cell renal cell carcinoma (ccRCC) mediated by 8 genes contained in the 3p21.3 tumor suppressor gene cluster and their effects on TME cell infiltration based on the TCGA database. The risk score model was established by principal component analysis. The hub gene NPRL2 was selected by protein-protein interactions (PPI) analysis. The effect of NPRL2 on sunitinib sensitivity of ccRCC was verified by using CCK-8, colony formation assay, wound healing assay, transwell assay and xenograft tumor model. Changes in protein expression were detected by Western blotting. We found that 8 TSGs were all differentially expressed in ccRCC samples, which could divide ccRCC into two subtypes. The constructed risk score model could predict the prognosis and drug sensitivity of ccRCC patients, and was an independent prognostic factor for ccRCC. Over-expression of NPRL2 promoted apoptosis, inhibited EMT, decreased the phosphorylation of the PI3K/AKT/mTOR signaling pathway to inhibit its activity, and promoted the sensitivity of sunitinib to ccRCC cells. Collectively, our findings increased the understanding of TSGs in ccRCC, suggesting that NPRL2 as a TSG could enhance sunitinib sensitivity to ccRCC cells.
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