ArticleInternational journal of clinical and experimental pathology2019
miR-5582-5p inhibits cell proliferation of non-small cell lung cancer through targeting FGF-10.
Article in International journal of clinical and experimental pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- Fibroblast Growth Factor Receptors (FGFRs) and Noncanonical Partners in Cancer Signaling.Cells · 2021Review
- Review
- Early diagnostic and prognostic value of serum exosomal miR-1246 in non-small cell lung cancer.International journal of clinical and experimental pathology · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence has suggested that microRNAs (miRNAs) play important roles in regulating the progression of cancerby acting as tumor suppressors or oncogenes. Here, our results demonstrated that miR-5582-5p was significantly down-regulated in non-small cell lung cancer (NSCLC) tissues and cell lines compared with normal controls. Overexpression of miR-5582-5p markedly inhibited the proliferation and migration of NSCLC cells. Consistently, the apoptosis of NSCLC cells was also significantly promoted by overexpressed miR-5582-5p. Functional study uncovered that miR-5582-5p bound the 3'-untranslated region (UTR) of fibroblastic growth factor-10 (FGF-10) and decreased the expression of FGF-10 in NSCLC cells. FGF-10 was up-regulated in NSCLC tissues and inversely correlated with the level of miR-5582-5p in NSCLC tissues. Overexpression of FGF-10 significantly reversed the inhibitory effect of miR-5582-5p on the proliferation of NSCLC cells. Taken together, our results demonstrated the functional mechanism of miR-5582-5p in suppressing malignant behaviors of NSCLC cells by targeting FGF-10. These findings demonstrated that miR-5582-5p might be a novel therapeutic target in the treatment of NSCLC.
Indexed as
Identifiers
31933923PMC6945143W3012117977What OpenQuestion holds
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.