ArticleCancer cell international2020
miR-363 suppresses the proliferation, migration and invasion of clear cell renal cell carcinoma by downregulating S1PR1.
Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Celecoxib suppresses colorectal cancer growth by inhibiting propionyl-CoA carboxylase alpha chain-mediated epithelial-mesenchymal transition and angiogenesis.Gastroenterology report · 2026Article
- Targeting miRNAs in renal cell carcinoma: emerging therapeutic strategies.International journal of clinical oncology · 2025Review
- Role of microRNA-363 during tumor progression and invasion.Journal of physiology and biochemistry · 2024Review
- Comprehensive cataloging of miR-363 as a therapeutic & non-invasive biomarker of prostate cancer.The Indian journal of medical research · 2024Article
- Non-coding RNAs as therapeutic targets in cancer and its clinical application.Journal of pharmaceutical analysis · 2024Review
- C-type lectin 2D (CLEC2D) is upregulated in clear cell renal cell carcinoma (ccRCC) tissues and predicts poor prognosis.Heliyon · 2024Article
- MiR-532-3p suppresses cell viability, migration and invasion of clear cell renal cell carcinoma through targeting TROAP.Cell cycle (Georgetown, Tex.) · 2021Article
- A Review of Recent Research on the Role of MicroRNAs in Renal Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2021Review
- Propofol inhibits the proliferation, migration, invasion and epithelial to mesenchymal transition of renal cell carcinoma cells by regulating microRNA-363/Snail1.American journal of translational research · 2021Article
- The Regulating Effect of Autophagy-Related MiRNAs in Kidney, Bladder, and Prostate Cancer.Journal of oncology · 2021Review
- Identification of Acute Myeloid Leukemia Bone Marrow Circulating MicroRNAs.International journal of molecular sciences · 2020Article
- MicroRNA Signature in Renal Cell Carcinoma.Frontiers in oncology · 2020Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMicroRNAs (miRNAs) serve as important regulators of the tumorigenesis and progression of many human cancers. Therefore, we evaluated the biological function and underlying mechanism of miR-363 in clear cell renal cell carcinoma (ccRCC).
methodsThe expression of miR-363 in ccRCC tissues compared with adjacent normal renal tissues was detected by quantitative real-time polymerase chain reaction, and the association between miR-363 levels and prognosis of ccRCC patients was analyzed. The candidate target gene of miR-363 was determined by in silico analysis and luciferase reporter assays. The effects of miR-363 on the proliferation, migration and invasion of ccRCC cells in vitro were determined by MTS assay, colony formation assay, Transwell assay and wound healing assay. We also investigated the roles of miR-363 in vivo by a xenograft tumour model. The mechanism of miR-363 on the proliferation, migration and invasion of ccRCC was determined by gain- and loss-of-function analyses.
resultswe demonstrated that miR-363 expression was obviously downregulated in ccRCC tissues and that reduced miR-363 expression was correlated with poor disease-free survival (DFS) in ccRCC patients after surgery. S1PR1 expression was inversely correlated with the level of miR-363 in human ccRCC samples. Luciferase reporter assays suggested that S1PR1 was a direct functional target of miR-363. miR-363 downregulated S1PR1 expression and suppressed the proliferation, migration and invasion abilities of ccRCC cells in vitro and suppressed xenograft tumour growth in vivo. Importantly, miR-363 exerted its biological function by inhibiting S1PR1 expression in ccRCC cells, leading to the repression of ERK activation. Moreover, we found that the levels of downstream effectors of ERK, including PDGF-A, PDGF-B, and epithelial-mesenchymal transition (EMT)-related genes, were decreased after miR-363 overexpression.
conclusionsOur results suggest that miR-363 acts as a tumour suppressor by directly targeting S1PR1 in ccRCC and may be a potential new therapeutic target for ccRCC.
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