ArticleOncotarget2015
Secreted uPAR isoform 2 (uPAR7b) is a novel direct target of miR-221.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- High uPAR and Low miR-221 Expression Predict Poor Disease-Free Survival in Triple-Negative Breast Cancer.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Article
- Posttranscriptional Regulation of the Plasminogen Activation System by Non-Coding RNA in Cancer.International journal of molecular sciences · 2023Review
- The functional significance and cross-talk of non-coding RNAs in triple negative and quadruple negative breast cancer.Molecular biology reports · 2022Review
- miR-221/222 as biomarkers and targets for therapeutic intervention on cancer and other diseases: A systematic review.Molecular therapy. Nucleic acids · 2022Review
- The Anticancer Effects of Flavonoids through miRNAs Modulations in Triple-Negative Breast Cancer.Nutrients · 2021Review
- Article
- MiRNA and LncRNA as Potential Biomarkers in Triple-Negative Breast Cancer: A Review.Frontiers in oncology · 2020Review
- Article
- Biomarker significance of plasma and tumor miR-21, miR-221, and miR-106a in osteosarcoma.Oncotarget · 2017Article
- uPAR enhances malignant potential of triple-negative breast cancer by directly interacting with uPA and IGF1R.BMC cancer · 2016Article
- Exploring miRNA-Associated Signatures with Diagnostic Relevance in Glioblastoma Multiforme and Breast Cancer Patients.Journal of clinical medicine · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
miR-221/-222 and components of the urokinase-type plasminogen activator system (uPAS) are associated with metastasis and poor prognosis in breast cancer, including the triple-negative subtype (TNBC). Modification of components of uPAS and involved miRNAs may contribute to targeted therapy for breast cancer patients. miR-221-/-222-overexpressing or miR-221-depleted cells were employed for qRT-PCR and Western blots to show associations of uPAR with miR-221/-222. To substantiate direct targeting of miR-221/-222 within 3' UTR of the uPAR isoform 2, in silico analysesand in vitro assays were conducted. Significant associations between miR-221 and uPAR isoform 2 expressions were observed at the mRNA and protein levels in breast cancer cells representing TNBC. For the first time, the uPAR isoform 2 was demonstrated as direct target for miR-221/-222. Inhibition of miR-221 reduced uPAR protein expression and expression of the tumor cell invasion markers vimentin and RHOC. These results demonstrate a direct and positive regulation of the secreted uPAR isoform 2 by miR-221, increasing its protein expression, a prerequisite for malignancy, while the other uPAR isoforms (1, 3 and 4) are indirectly regulated through miR-10b and miR-221/-222. By targeting uPAR isoforms and/or miRNA-221/-222, the diagnosis and therapy of breast cancer, in particular in TNBC, could be significantly improved.
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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.