ArticleCancer medicine2019
miR-107 regulates growth and metastasis of gastric cancer cells via activation of the PI3K-AKT signaling pathway by down-regulating FAT4.
Article in Cancer medicine, 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 It has been retracted, and should not be counted.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 35 papers.
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Who cites it
35 citing papers in PubMed, 52 citations in OpenAlex.
- TET1-mediated DNA demethylation and transcription activation of MRPS17 induces lung adenocarcinoma through PI3K-AKT-mTOR pathway.Journal of molecular histology · 2026Article
- The paradox of miR-107 in oncology: dual roles as a tumor suppressor and oncomiR.Cancer gene therapy · 2026Review
- RETRACTION: miR-107 Regulates Growth and Metastasis of Gastric Cancer Cells via Activation of the PI3K-AKT Signaling Pathway by Down-Regulating FAT4.Cancer medicine · 2026Article
- Application of serum miRNA panel in bladder cancer detection.Translational andrology and urology · 2026Article
- MicroRNA-107 alleviates ferroptosis-mediated acute kidney injury by regulating the PI3K/Akt/mTOR pathway.BMC nephrology · 2025Article
- UBE4B promotes gastric cancer proliferation and metastasis by mediating FAT4 ubiquitination and degradation.Cell death & disease · 2025Article
- Vincristine exerts antiglioma effects by inhibiting the PI3K/AKT signaling pathway: A mechanistic study based on network pharmacology, bioinformatics analysis, and experimental validation.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Prognostic implications of microRNA-107 in esophageal cancer: a retrospective cohort study.PeerJ · 2025Article
- Global Transcriptomic Analysis of Topical Sodium Alginate Protection against Peptic Damage in an In Vitro Model of Treatment-Resistant Gastroesophageal Reflux Disease.International journal of molecular sciences · 2024Article
- Non-Coding RNA as Biomarkers and Their Role in the Pathogenesis of Gastric Cancer-A Narrative Review.International journal of molecular sciences · 2024Review
- Enhancing protein production and growth in chinese hamster ovary cells through miR-107 overexpression.AMB Express · 2024Article
- FAT4 Mutation is Related to Tumor Mutation Burden and Favorable Prognosis in Gastric Cancer.Current genomics · 2024Article
- Exploring the mechanism of ellagic acid against gastric cancer based on bioinformatics analysis and network pharmacology.Journal of cellular and molecular medicine · 2023Article
- FAT4 expression in peripheral blood mononuclear cells is associated with prognosis and immune cell infiltration in hepatocellular carcinoma.Scientific reports · 2023Article
- miRNAs as prognostic predictors in acute myeloid leukemia.Translational cancer research · 2023Article
- High expression of miR-107 and miR-17 predicts poor prognosis and guides treatment selection in acute myeloid leukemia.Translational cancer research · 2023Article
- Increased expression of FAT4 suppress metastasis of lung adenocarcinoma through regulating MAPK pathway and associated with immune cells infiltration.Cancer medicine · 2023Article
- Chromatin and noncoding RNA-mediated mechanisms of gastric tumorigenesis.Experimental & molecular medicine · 2023Review
- DSCR9/miR-21-5p axis inhibits pancreatic cancer proliferation and resistance to gemcitabine via BTG2 signaling.Acta biochimica et biophysica Sinica · 2022Article
- miR-107 Inhibits the Proliferation of Gastric Cancer CellsFrontiers in genetics · 2022Article
Corrections and comments
- Retracted
Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo investigate the effect of miR-107 on the growth and metastasis of gastric cancer (GC) and elucidate the probable mechanisms.
methodsThe expression of miR-107 and FAT4 in GC tissues and cells were detected using qRT-PCR. Bioinformatics and dual luciferase reporter gene assays were used to analyze the relationship between miR-107 and FAT4. miR-NC, miR-107 inhibitor, pcDNA3.1-FAT4 and siRNA-FAT4 were transfected into AGS and MKN-45 GC cell lines, respectively. The proliferation and migration abilities of GC cells after transfection were evaluated using the MTT assay, scratch test and transwell assay. The expression of epithelial-mesenchymal transition (EMT) markers: E-cadherin, N-cadherin, vimentin and related proteins of the PI3K/AKT signaling pathway were determined using western blot. The xenograft tumors of nude mice were observed to assess the tumorigenicity of GC cells in vivo.
resultsMiR-107 was up-regulated, while FAT4 was down-regulated in GC tissues and cells (P < 0.05); FAT4 was targeted and negatively regulated by miR-107. Down-regulating miR-107 or up-regulating FAT4 inhibited the GC cells proliferation, migration, invasion and tumorigenicity, and could also reduce the expression of N-cadherin, vimentin, p-PI3K and p-Akt expression and up-regulate E-cadherin.
conclusionsmiR-107 promotes growth and metastasis in GC via activation of PI3K-AKT signaling by targeting FAT4, which may be a target for GC treatment.
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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.