ArticleCancer cell international2025
MicroRNA profiling identifies VHL/HIF-2α dependent miR-2355-5p as a key modulator of clear cell Renal cell carcinoma tumor growth.
Article in Cancer cell international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- Regulatory networks of non-coding RNAs in renal cell carcinogenesis and therapeutic intervention strategies.World journal of urology · 2026Review
- Kidney-specific HIF-1α-dependent ARL10/miR-1271-5p overexpression in clear cell renal cell carcinoma.British journal of cancer · 2026Article
- Integrated Transcriptomic Analysis Identifies a Six-Gene Prognostic Signature, RNA Editing Derived Neoantigens, and miRNA Regulatory Networks in Renal Cell Carcinoma.Iranian journal of medical sciences · 2026Article
- Short and Long Non-Coding RNAs in Renal Cell Carcinoma.Non-coding RNA · 2026Review
- Research progress ofFrontiers in immunology · 2026Review
- Article
- ALDOB is a prognostic biomarker and a potential immunotherapy target for clear cell renal cell carcinoma.PeerJ · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Inactivation of the von Hippel-Lindau (VHL) tumor suppressor gene is one of the first truncal events in clear cell Renal Cell Carcinoma (ccRCC) tumorigenesis. The accumulation of Hypoxia Induced Factor (HIFα) resulting from VHL loss can promote ccRCC tumorigenesis by regulating microRNA (miRNA) expression. Here, we performed miRNA profiling and high-throughput analysis to identify a panel of VHL-dependent miRNAs in ccRCC. Validation of these miRNAs revealed the overexpression of miR-2355-5p in ccRCC cell models and primary tumors. Moreover, we showed a significant increase in circulating miR-2355-5p in plasma from patients with ccRCC. Mechanistically, miR-2355-5p overexpression was confirmed to be HIF-2α dependent. Targeting miR-2355-5p with the CRISPR/Cas9 system not only negatively disrupted the ability of ccRCC cells to stimulate angiogenesis but also decreased cell proliferation and drastically reduced tumor growth in mouse xenograft models. Finally, a miR-2355-5p pulldown assay identified five tumor suppressor genes, ACO1, BTG2, CMTM4, SLIT2, and WDFY2, as potential targets. All five genes were significantly downregulated in ccRCC tumors and mouse xenograft tumors. The results from this research demonstrate the oncogenic ability of miR-2355-5p and shed light on the possible mechanism by which this miRNA controls angiogenesis and tumor growth in VHL-deficient ccRCC.
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