ArticleOncoTargets and therapy2021
MiR-17 and miR-93 Promote Tumor Progression by Targeting p21 in Patients with Chordoma.
Article in OncoTargets and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- DDX3 participates in miRNA biogenesis and RNA interference through translational control of PACT and interaction with AGO2.FEBS open bio · 2025Article
- Dysregulation of noncoding RNA in chordoma; implications in identifying potential targets for novel therapeutic approaches.Molecular biology reports · 2024Review
- XIST sponges miR-320d to promote chordoma progression by regulating ARF6.Journal of bone oncology · 2022Article
- miRNAs as Biomarkers and Possible Therapeutic Strategies in Synovial Sarcoma.Frontiers in pharmacology · 2022Review
- CMTM3 suppresses chordoma progress through EGFR/STAT3 regulated EMT and TP53 signaling pathway.Cancer cell international · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveMicroRNAs have been implicated in the progression of various cancers. However, the role of microRNAs in chordoma remains to be further elucidated. Here, we purposed to character the role of two microRNAs, miR-17 and miR-93, and their potential mechanisms in chordoma.
methodsThe expression and prognostic value of miR-17 and miR-93 were assessed by the quantitative real-time polymerase chain reaction, Kaplan-Meier survival curve, and Cox regression analysis. The effects of miR-17/93 mimics on chordoma cell proliferation, colony formation, and invasion were analyzed by CCK-8 assay, colony formation assay, and transwell assay. The downstream target of miR-17/93 was further explored via luciferase reporter assay.
resultsHigh expression of miR-17/93 was identified in chordoma tissues, and was associated with poor prognosis. Overexpression of miR-17/93 contributed to cell proliferation, colony formation, and invasion. Mechanistically, we demonstrated that miR-17/93 directly targeted p21 and decreased the expression of p21. Besides, the rescue assay further confirmed the essential role of the miR-17/93-p21 axis in chordoma.
conclusionOur results revealed the potential oncogenic effect of the miR-17/93 on chordoma progression, and suggested that the miR-17/93-p21 axis served as a promising therapeutic target in chordoma.
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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 Socratic graph.