ArticlePloS one2015
MicroRNA-206: Effective Inhibition of Gastric Cancer Progression through the c-Met Pathway.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 38 citations in OpenAlex.
- Unveiling promising targets in gastric cancer therapy: A comprehensive review.Molecular therapy. Oncology · 2024Review
- Research progress on the development of hepatocyte growth factor/c-Met signaling pathway in gastric cancer: A review.World journal of gastrointestinal oncology · 2024Review
- Ferroptosis regulating lipid peroxidation metabolism in the occurrence and development of gastric cancer.World journal of gastrointestinal oncology · 2024Article
- Non-coding RNAs as potential therapeutic targets for receptor tyrosine kinase signaling in solid tumors: current status and future directions.Cancer cell international · 2024Review
- Interaction between miR‑206 and lncRNA MALAT1 in regulating viability and invasion in hepatocellular carcinoma.Oncology letters · 2024Article
- Crizotinib-based proteolysis targeting chimera suppresses gastric cancer by promoting MET degradation.Cancer science · 2023Article
- Integrated pan-cancer analysis and experimental verification of the roles of tropomyosin 4 in gastric cancer.Frontiers in immunology · 2023Article
- Article
- c-Met: A Promising Therapeutic Target in Bladder Cancer.Cancer management and research · 2022Review
- miR-206 inhibits liver cancer stem cell expansion by regulating EGFR expression.Cell cycle (Georgetown, Tex.) · 2020Article
- Targeting the HGF/MET Axis in Cancer Therapy: Challenges in Resistance and Opportunities for Improvement.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
- MicroRNAs and Long Non-coding RNAs in c-Met-Regulated Cancers.Frontiers in cell and developmental biology · 2020Review
- Review
- The long non-coding RNA-ROR promotes osteosarcoma progression by targeting miR-206.Journal of cellular and molecular medicine · 2019Article
- Retracted Article: MiR-206 reduced the malignancy of hepatocellular carcinoma cellsRSC advances · 2019Article
- LncRNA RMRP silence curbs neonatal neuroblastoma progression by regulating microRNA-206/tachykinin-1 receptor axis via inactivating extracellular signal-regulated kinases.Cancer biology & therapy · 2019Article
- HGF/c-MET: A Promising Therapeutic Target in the Digestive System Cancers.International journal of molecular sciences · 2018Review
- Cancer prevention through miRNAs: miR-206 prevents the initiation and progression of hepatocellular carcinoma by attenuating c-MET signaling and cell-cycle progression via cyclin D1 and CDK6.Non-coding RNA investigation · 2018Article
- Cigarette smoke enhances oncogene addiction to c-MET and desensitizes EGFR-expressing non-small cell lung cancer to EGFR TKIs.Molecular oncology · 2018Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs are endogenous short chain nucleotide RNAs that regulate gene function by direct binding of target mRNAs. In this study, we investigated the effects of microRNA-206 (miR-206) on the development of gastric cancer. miR-206 was first confirmed to be downregulated in gastric cancer specimens. Conversely, upregulation of c-Met was confirmed in tissue samples of human gastric cancer, with its level inversely correlated with miR-206 expression. Introduction of miR-206 inhibited cellular proliferation by inducing G1 cell cycle arrest, as well as migration and invasion. Moreover, important proliferation and/or migration related molecules such as c-Met, CDK4, p-Rb, p-Akt and p-ERK were confirmed to be downregulated by Western blot analysis. Targeting of c-Met also directly affected AGS cell proliferation, migration and invasion. In vivo, miR-206 expressing tumor cells also displayed growth delay in comparison to unaffected tumor cells. Our results demonstrated that miR-206 suppressed c-Met expression in gastric cancer and could function as a potent tumor suppressor in c-Met overexpressing tumors. Inhibition of miR-206 function could contribute to aberrant cell proliferation and migration, leading to gastric cancer development.
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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.