ArticleMolecular medicine reports2019
MicroRNA‑206 exerts anti‑oncogenic functions in esophageal squamous cell carcinoma by suppressing the c‑Met/AKT/mTOR pathway.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 11 papers, 1 of them a synthesis that pooled it.
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
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Prognostic Value and Clinicopathological Features of MicroRNA-206 in Various Cancers: A Meta-Analysis.BioMed research international · 2020Pooled it
- 'Investigation of miRNAs That Affect the PI3K/AKT/mTOR Signaling Pathway in Endometrial Cancer'.Cell biochemistry and biophysics · 2025Article
- MicroRNAs: A novel signature in the metastasis of esophageal squamous cell carcinoma.World journal of gastroenterology · 2024Review
- Interaction between miR‑206 and lncRNA MALAT1 in regulating viability and invasion in hepatocellular carcinoma.Oncology letters · 2024Article
- Review
- Urinary microRNA biomarkers for detecting the presence of esophageal cancer.Scientific reports · 2021Article
- The regulatory relationship and function of LncRNA FAM225A-miR-206-ADAM12 in gastric cancer.American journal of translational research · 2021Article
- PRR11 and SKA2 promote the proliferation, migration and invasion of esophageal carcinoma cells.Oncology letters · 2020Article
- MicroRNAs and Long Non-coding RNAs in c-Met-Regulated Cancers.Frontiers in cell and developmental biology · 2020Review
- Crosstalk Mechanisms Between HGF/c-Met Axis and ncRNAs in Malignancy.Frontiers in cell and developmental biology · 2020Review
- Emerging Role of Non-Coding RNAs in Esophageal Squamous Cell Carcinoma.International journal of molecular sciences · 2019Review
Corrections and comments
- Retraction · 2025-11-25Author Unresponsive · Concerns/Issues about Data · Euphemisms for Plagiarism · Investigation by Journal/Publisher · Investigation by Third Party · Plagiarism of Data · · See also: https://pubpeer.com/publications/E7C9F60DED7334691C6EE591988EBB
- Retracted
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence suggests that the dysregulation of microRNAs (miRNAs) has an important role in the progression of human cancer, including ESCC. However, the exact functions and mechanisms of miRNAs in ESCC remain largely unclear. The aim of the present study was to investigate the expression and biological functions of miRNAs in ESCC and reveal the underlying molecular mechanisms. miRNA microarray and reverse transcription‑quantitative polymerase chain reaction analyses were performed, which identified and confirmed that miR‑206 was significantly downregulated in ESCC tissues and cell lines. Its low expression was associated with lymph node metastasis, advanced TNM stage and N classification, as well as poorer overall survival in patients with ESCC. CCK‑8 and flow cytometry assays demonstrated that ectopic miR‑206 expression inhibited ESCC cell proliferation and induced cell apoptosis. In addition, MET proto‑oncogene, receptor tyrosine kinase (c‑Met), a well‑known oncogene, was a direct target of miR‑206. An inverse correlation between the levels of miR‑206 and c‑Met mRNA in ESCC tissue samples was confirmed. Notably, c‑Met overexpression inhibited the effects of miR‑206 on the proliferation and apoptosis of ESCC cells. Additionally, it was confirmed that the tumor‑suppressive functions of miR‑206 may have contributed to the inactivation of the c‑Met/protein kinase B (AKT)/mechanistic target of rapamycin (mTOR) signaling pathway. In conclusion, the findings of the present study suggested that miR‑206 exerts its anti‑cancer functions via the c‑Met/AKT/mTOR signaling pathway, providing a novel candidate prognostic factor and a potential therapeutic target in ESCC.
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What 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.