ArticleAging2024
The role of miR-6884-5p in epithelial-mesenchymal transition in non-small cell lung cancer.
Article in Aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed, 3 citations in OpenAlex.
- Mechanisms of microRNA Regulation of the Epithelial-Mesenchymal Transition (EMT) in Lung Cancer.Life (Basel, Switzerland) · 2024Review
- miR-6884-5p inhibits proliferation and epithelial-mesenchymal transition in non-small cell lung cancer cells.Heliyon · 2024Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Significant progress has been made in the management of non-small cell lung cancer (NSCLC), though a big barrier remains, which is epithelial-mesenchymal transition (EMT). Our study aimed to evaluate the function of miR-6884-5p and S100A16 in EMT-aggravated NSCLC. The tumor tissues and adjacent tissues from 92 NSCLC patients were collected to analyze the expression of miR-6884-5p and S100A16. Then lung cancer cell line A549 was co-transfected with miR-6884-5p mimics and S100A16 to further evaluate their function. Compared to adjacent tissues, low expression of miR-6884-5p was observed in the NSCLC tissues and associated with severe NSCLC progression. MiR-6884-5p expression was negatively correlated with EMT in NSCLC. Luciferase assay data revealed that miR-6884-5p could directly bind to the 3'UTR of S100A16 and inhibited the expression of S100A16 in A549 cells. Moreover, miR-6884-5p mimics significantly ameliorated EMT progression, and overexpression of S100A16 could reverse the inhibitory effect of miR-6884-5p in A549 cells. MiR-6884-5p inhibited EMT through directly targeting S100A16 in NSCLC. Our findings suggest that miR-6884-5p could be a diagnostic marker of NSCLC, as well as a potential candidate for NSCLC treatment.
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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.