Abstract
Clear cell renal cell carcinoma (ccRCC) carrying wild-type Von Hippel–Lindau (VHL) tumor suppressor are more invasive and of high morbidity. Concurrently, competing endogenous RNA (ceRNA) network has been suggested to play an important role in ccRCC malignancy. In order to understand why the patients carrying wild-type VHL gene have high degrees of invasion and morbidity, we applied bioinformatics approaches to identify 861 differentially expressed RNAs (DE-RNAs) between patients carrying wild-type and patients carrying mutant VHL from The Cancer Genome Atlas (TCGA) database, established a ceRNA network including 122 RNAs, and elected six survival-related DE-RNAs including Linc00942, Linc00858, RP13_392I16.1, hsa-miR-182-5p, hsa-miR-183-5p, and PAX3. Examining clinical samples from our hospital revealed that patients carrying wild-type VHL had significantly higher levels of all six RNAs than those carrying mutant VHL. Patients carrying wild-type VHL had significantly higher risk scores, which were calculated based on expression levels of all six RNAs, than those carrying mutant VHL. Patients with higher risk scores had significantly shorter survival times than those with lower risk scores. Therefore, the risk scores serve well to predict malignancy and prognosis.
Highlights
Kidney cancer is one of the top 10 most common tumors, the second-ranked malignant tumor in urologic system, and contributes 2% to 3% of the human malignant tumors worldwide [1, 2]
We analyzed the levels of Long non-coding RNA (lncRNA), miRNAs, and messenger RNA (mRNA) between Clear cell renal cell carcinoma (ccRCC) patients carrying wild-type and those carrying mutant Von Hippel–Lindau (VHL) in The Cancer Genome Atlas (TCGA) database; displayed the distribution of those differentially expressed RNAs (DE-RNAs) in form of volcano map; and defined those RNAs with |log2foldchange| > 1 and Adj.p.val < 0.05 as DE-RNAs
Previous studies have revealed that the LINC01094 enhances the expression of miR184 and inhibits the expression of SLC2A3, which suppresses the development of ccRCC [27]
Summary
Kidney cancer is one of the top 10 most common tumors, the second-ranked malignant tumor in urologic system, and contributes 2% to 3% of the human malignant tumors worldwide [1, 2]. The inactivation of VHL gene alone is not sufficient to cause tumors [12, 13], a study of ccRCC patients from Germany suggested that low expression of VHL was identified as a risk factor for worse overall survival (OS) [14]. A recent study indicated that about 40%–60% of patients with sporadic ccRCC carry wild-type VHL, and such tumors are more invasive and lead to a dramatic reduction of survival rates as compared with those carrying mutant VHL [16, 17]. It is more urgent to identify other factors that are closely associated with patients’ survival in addition to VHL mutation
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