ArticleAnnals of translational medicine2021
CD248 as a bridge between angiogenesis and immunosuppression: a promising prognostic and therapeutic target for renal cell carcinoma.
Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.
- Immunosuppressive roles of pericytes in cancer disease: insights from a systematic review and meta-analysis.Journal of translational medicine · 2026Pooled it
- Immortalized smooth muscle cells enhance in vitro vasculogenesis.Angiogenesis · 2026Article
- Immortalized smooth muscle cells enhance in vitro vasculogenesis.Research square · 2026Article
- Mesangial angiogenesis and interstitial eosinophilic infiltration in diabetic nephropathy are associated with elevated CD248 expression.Renal failure · 2025Article
- Endosialin in Cancer: Expression Patterns, Mechanistic Insights, and Therapeutic Approaches.Theranostics · 2024Review
- TEM1 up-regulates MMP-2 and promotes ECM remodeling for facilitating invasion and migration of uterine sarcoma.Discover oncology · 2023Article
- Heterogeneity of Platelet Derived Growth Factor Pathway Gene Expression Profile Defines Three Distinct Subgroups of Renal Cell Carcinomas.Cancer genomics & proteomicsArticle
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRenal cell carcinoma (RCC) is characterized by significant vascularization and immunogenicity, which contributes to drug resistance and immune escape. CD248, a pericytes marker in tumor vasculature, might help explain tumor microenvironment (TME) remodeling and serve as a novel therapeutic target.
methodsTranscriptome data and clinical information of RCC patients were obtained from The Cancer Genome Atlas (TCGA) database. ESTIMATE and microenvironment cell population (MCP)-counter algorithms were adopted to calculate immune and stromal contents. The prognostic value of TME was evaluated via Kaplan-Meier and Wilcoxon signed rank test. Pearson's correlation coefficient was employed to explore the correlation between angiogenesis and TME, and the relationship between CD248 and TME or RCC progression. CD248 overexpression and vascular colocalization in RCC were confirmed via histology staining. The weighted gene coexpression network analysis (WGCNA) and enrichment analysis were performed to explore CD248-mediated regulatory mechanism in angiogenesis and TME remodeling. CD248-based drug response was predicted through CellMiner database.
resultsTumor angiogenesis contributed to deteriorated RCC progression, which might be involved with immunosuppression. More specifically, upregulated immune checkpoints exhausted infiltrated T cells. CD248 overexpressed in RCC vessels correlated with TME and predicted a bad survival outcome. CD248 and coexpressed genes participated in angiogenesis and TME remodeling. Several clinical approved drugs that might inhibit CD248-mediated tumor promoting effects were selected.
conclusionsCD248 appears to contribute to angiogenesis and immunosuppressive TME, and may thus be a promising prognostic and therapeutic target for RCC. CD248-based medication guidance might benefit RCC patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.