ArticleCell stress & chaperones2021
Mechanism of miR-455-3 in suppressing epithelial-mesenchymal transition and angiogenesis of non-small cell lung cancer cells.
Article in Cell stress & chaperones, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 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
3 citing papers in PubMed, 9 citations in OpenAlex.
- miRNA/mRNA analysis of increased TGF-β pathways drive epithelial-mesenchymal transition and regulatory T cell differentiation.Frontiers in immunology · 2026Article
- miRNA/mRNA analysis of increased TGF-β pathways drive epithelial-mesenchymal transition and regulatory T cell differentiation.bioRxiv : the preprint server for biology · 2025Article
- Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor-suppressing role of miR-455-3p has been reported in lung cancer, but the working mechanism remains to be fully elucidated. This study aims to explore the possible mechanism of miR-455-3p in regulating epithelial-mesenchymal transition (EMT) progression and angiogenesis in non-small cell lung cancer (NSCLC) cells.The expressions of miR-455-3p, HSF1, GLS1, and EMT-related proteins (E-cadherin, N-cadherin, vimentin, and Snail-1) in both NSCLC tissues and cell lines were determined by RT-qPCR and western blot. After cell transfection, cell proliferation and angiogenesis ability on NSCLC cells were assessed by MTT and tube formation assay. The binding of miR-455-3p with HSF1 was measured by luciferase reporter gene assay, while the interaction between HSF1 and GLS1 was determined by co-immunoprecipitation assay (Co-IP).HSF1 was highly expressed in NSCLC tissues and cells. Inhibition of HSF1 expression or overexpression of miR-455-3p in NSCLC cells can suppress cell proliferation, angiogenesis ability, and EMT progression. miR-455-3p was found to negatively regulate HSF1 expression. Co-transfection of miR-455-3p overexpression and HSF1 inhibition in NSCLC cells showed that miR-455-3p can partially counteract the effect of HSF1 in NSCLC cells. HSF1 can interact with GLS1 and elevate the expression of GLS1. GLS1 can partially abolish the suppressive effect of miR-455-3p in NSCLC cells.miR-455-3p can bind HSF1 to suppress the GLS1 in NSCLC cells, therefore suppressing EMT progression and angiogenesis of NSCLC cells.
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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.