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Published on: February 20, 2019
SEL1L3 as a link molecular between renal cell carcinoma and atherosclerosis based on bioinformatics analysis and
Haoyuan Wang1, Xiaopeng Ma2, Sijie Li1
1Department of Urology Surgery, The Fourth Hospital of Hebei Medical University, Shijiazhuang 050011, Hebei Province, China.
Background:
Renal cancer, the most common type of kidney cancer, develops in the renal tubular epithelium. Atherosclerosis of the aorta is the primary cause of atherosclerosis. However, the underlying mechanisms remain unclear.
Methods:
The renal clear cell carcinoma RNA sequence profile was obtained from The Cancer Genome Atlas (TCGA) database, and the atherosclerosis datasets GSE28829 and GSE43292 based on GPL570 and GPL6244 was obtained from the Gene Expression Omnibus (GEO) database. The difference and hub genes were identified by the Limma protein-protein interaction (PPI) network in R software. Functional enrichment, survival, and immunoinfiltration analyses were performed. The role of SEL1L3 in the ErbB/PI3K/mTOR signaling pathway, apoptosis, invasion, cell cycle, and inflammation was analyzed using western blotting.
Results:
764 DEGs were identified from TCGA Kidney Renal Clear Cell Carcinoma (KIRC) dataset. A total of 344 and 117 DEGs were screened from the GSE14762 and GSE53757 datasets, respectively. Functional enrichment analysis results primarily indicated enrichment in the transporter complex, DNA-binding transcription activator activity, morphogenesis of the embryonic epithelium, stem cell proliferation, adrenal overactivity and so on. Fifteen common DEGs overlapped among the three datasets. The PPI network revealed that SEL1L3 was the core gene. Survival analysis showed that lower SEL1L3 expression levels led to a worse prognosis. Immune cell infiltration analysis showed that SEL1L3 expression was significantly correlated with antibody-drug conjugates (aDC), B cells, eosinophils, interstitial dendritic cells (iDC), macrophages, and more.
Conclusions:
SEL1L3 plays an important role in renal clear cell carcinoma and atherosclerosis and may be a potential link between them.
Insights
SEL1L3 is a key gene in kidney renal clear cell carcinoma and atherosclerosis. Its lower expression correlates with poorer prognosis, suggesting it may link these two conditions.
Area of Science:
- Oncology
- Cardiovascular Biology
- Genomics
Background:
- Renal clear cell carcinoma originates in the renal tubular epithelium.
- Atherosclerosis of the aorta is a primary cause of atherosclerosis, but mechanisms are unclear.
Purpose of the Study:
- To investigate the role of SEL1L3 in renal clear cell carcinoma and atherosclerosis.
- To identify potential molecular links between these two conditions.
Main Methods:
- Utilized The Cancer Genome Atlas (TCGA) for renal clear cell carcinoma RNA sequencing and Gene Expression Omnibus (GEO) for atherosclerosis datasets.
- Employed Limma and protein-protein interaction (PPI) network analysis to identify differentially expressed and hub genes.
- Conducted functional enrichment, survival, and immune cell infiltration analyses, alongside western blotting for pathway analysis.
Main Results:
- Identified 15 common differentially expressed genes (DEGs) across three datasets, with SEL1L3 identified as a core gene.
- Lower SEL1L3 expression was associated with a worse prognosis in renal clear cell carcinoma.
- SEL1L3 expression correlated significantly with immune cell infiltration, including B cells and macrophages.
Conclusions:
- SEL1L3 plays a significant role in both renal clear cell carcinoma and atherosclerosis.
- SEL1L3 may represent a potential molecular link connecting kidney cancer and aortic atherosclerosis.
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