ArticleMolecular medicine reports2019
MicroRNA‑212 facilitates the motility and invasiveness of esophageal squamous carcinoma cells.
Article in Molecular medicine reports, 2019. 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.
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
5 citing papers in PubMed, 6 citations in OpenAlex.
- Extracellular RNA in oncogenesis, metastasis and drug resistance.RNA biology · 2024Review
- Targeting Strategies for Aberrant Lipid Metabolism Reprogramming and the Immune Microenvironment in Esophageal Cancer: A Review.Journal of oncology · 2022Review
- Current Advances inFrontiers in pharmacology · 2021Review
- MiR-212-3p mediates apoptosis and invasion of esophageal squamous cell carcinoma through inhibition of the Wnt/β-catenin signaling pathway by targeting SOX4.Journal of thoracic disease · 2020Article
- Esophageal Microenvironment: From Precursor Microenvironment to Premetastatic Niche.Cancer management and research · 2020Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a tumor‑associated microRNA (miR), miR‑212 has dual functions; either as an oncogene or a tumor suppressor. A high expression level of miR‑212 was reported to be associated with poor outcome in patients with esophageal squamous cell carcinoma (ESCC), however, its role in ESCC progression has not been explored. In the present study, an in vitro cell model of lentivirus‑mediated gain‑of‑function demonstrated promotion of ESCC cell migration and invasion when miR‑212 was overexpressed, and no effect on cell proliferation. miR‑212 resulted in downregulation of the expression of E‑cadherin, β‑catenin, vimentin and Twist1. Moreover, it led to increased levels of extracellular matrix (ECM)‑degrading enzymes, matrix metalloproteinase‑9 and urokinase‑type plasminogen activator. Furthermore, berberine inhibited miR‑212‑induced ESCC cell migration, unlike the PI3K inhibitor LY294002, rapamycin (mTOR inhibitor), 5‑(Tetradecyloxy)‑2‑furoic acid (TOFA; an acetyl‑CoA carboxylase 1 inhibitor), metformin and propranolol. These data suggest that miR‑212 activates multiple signaling cascades and facilitates ESCC cell motility and invasion by promoting the epithelial‑mesenchymal transition and degrading the ECM. Berberine may be a potential therapeutic agent against metastasis in patients with ESCC, who express high levels of miR‑212.
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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.