ArticleJournal of clinical laboratory analysis2022
MiR-630 suppresses non-small cell lung cancer by targeting vimentin.
Article in Journal of clinical laboratory analysis, 2022. 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, 16 citations in OpenAlex.
- Clinical significance of miR-3178 in non-small cell lung cancer patients.Journal of medical biochemistry · 2026Article
- MicroRNAs in Esophageal Cancer: Implications for Diagnosis, Progression, Prognosis and Chemoresistance.International journal of molecular sciences · 2026Review
- LINC01559 promotes lung adenocarcinoma metastasis by disrupting the ubiquitination of vimentin.Biomarker research · 2024Article
- MiR-630 suppresses non-small cell lung cancer by targeting vimentin.Journal of clinical laboratory analysis · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveThis study aimed to clarify the function of miR-630 on non-small cell lung cancer (NSCLC) cells.
methodsQuantitative real-time PCR was utilized to detect the mRNA expression of miR-630 and vimentin (VIM) in NSCLC tissues and cells. The protein expression of VIM, P53, Caspase-3, Bcl-2, Bax and JAK2/STAT3 was evaluated via Western blot. Dual-luciferase reporter assay was applied to evaluate whether VIM is the target gene of miR-630. The migration, invasion, proliferation and apoptosis of NSCLC cells were examined by wound-healing assay, transwell assay, CCK-8 assay, and flow cytometry, respectively.
resultsMiR-630 was lowly expressed in NSCLC tissues and cells, while VIM was highly expressed in NSCLC cells. Dual-luciferase reporter assay data validated that miR-630 directly targeted VIM. MiR-630 overexpression inhibited VIM expression, but the inhibition of miR-630 upregulated VIM expression. Besides, miR-630 mimics restrained cell migration, invasion, and proliferation, and promoted NSCLC cell apoptosis. Whereas, VIM overexpression partly attenuated the inhibitory effect of miR-630 on NSCLC cells. Moreover, miR-630 mimics impeded p-JAK2 and p-STAT3 protein expression; and miR-630 inhibitor upregulated p-STAT3 and VIM protein expression, which was reversed after the addition of STAT3 inhibitor C188-9.
conclusionMiR-630 constrained the progression of NSCLC by inhibiting JAK2/STAT3 pathway and downregulating VIM expression.
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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.