ArticleOncotarget2016
MiR-206 suppresses epithelial mesenchymal transition by targeting TGF-β signaling in estrogen receptor positive breast cancer cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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.
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Who cites it
43 citing papers in PubMed, 72 citations in OpenAlex.
- Circulating MicroRNA in Breast Cancer.Cancers · 2026Review
- New microRNA-based therapies reveal common targets in paediatric medulloblastoma and adult glioblastoma.Scientific reports · 2025Article
- RNA signaling in skeletal muscle: the central role of microRNAs and exosomal microRNAs.Frontiers in cell and developmental biology · 2025Review
- Interaction between miR‑206 and lncRNA MALAT1 in regulating viability and invasion in hepatocellular carcinoma.Oncology letters · 2024Article
- Estrogen Receptor Signaling in Breast Cancer.Cancers · 2023Review
- ER Negative Breast Cancer and miRNA: There Is More to Decipher Than What the Pathologist Can See!Biomedicines · 2023Review
- Emerging roles and mechanisms of miR-206 in human disorders: a comprehensive review.Cancer cell international · 2022Review
- The Role of Abnormal Uterine Junction Zone in the Occurrence and Development of Adenomyosis.Reproductive sciences (Thousand Oaks, Calif.) · 2022Review
- The crosstalk between reactive oxygen species and noncoding RNAs: from cancer code to drug role.Molecular cancer · 2022Review
- hsa-miR-206b Involves in the Development of Papillary Thyroid Carcinoma via Targeting LMX1B.BioMed research international · 2022Article
- MicroRNA-206 suppresses growth and metastasis of breast cancer stem cells via blocking EVI-1-mediated CALR expression.PloS one · 2022Article
- MicroRNA-18a-5p represses scar fibroblast proliferation and extracellular matrix deposition through regulating Smad2 expression.Experimental and therapeutic medicine · 2021Article
- MicroRNA-206 has a bright application prospect in the diagnosis of cases with oral cancer.Journal of cellular and molecular medicine · 2021Article
- MicroRNAs' role in the environment-related non-communicable diseases and link to multidrug resistance, regulation, or alteration.Environmental science and pollution research international · 2021Review
- MicroRNA-206 inhibits the proliferation, migration and invasion of colorectal cancer cells by regulating the c-Met/AKT/GSK-3β pathway.Oncology letters · 2021Article
- Article
- Autocrine TGF-β in Cancer: Review of the Literature and Caveats in Experimental Analysis.International journal of molecular sciences · 2021Review
- miRNA Expression Profiles in Luminal A Breast Cancer-Implications in Biology, Prognosis, and Prediction of Response to Hormonal Treatment.International journal of molecular sciences · 2020Review
- Revisiting cancer hallmarks: insights from the interplay between oxidative stress and non-coding RNAs.Molecular biomedicine · 2020Review
- MiR-206 suppresses proliferation and epithelial-mesenchymal transition of renal cell carcinoma by inhibiting CDK6 expression.Human cell · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPrevious reports have shown a mutual negative feedback loop between microRNA (miR)-206 and estrogen receptor (ER) expression. Furthermore, decreased miR-206 expression in breast cancer (BC) is associated with the advanced clinical stage and lymph node metastasis. However, its role and the mechanism underlying the migration and invasion of ER positive BC remain unclear.
resultsIn this study, miR-206 was stably transfected into ER positive cell lines MCF-7 and T47D to investigate the effect of miR-206. The results showed that miR-206 overexpression markedly impaired the migration and invasive abilities of these cells, followed by suppression of the epithelial mesenchymal transition (EMT). Mechanistic analyses showed that miR-206 inhibited the autocrine production of transforming growth factor (TGF)-β as well as the downstream expression of neuropilin-1 (NRP1) and SMAD2, responsible for the decreased migration, invasion, and EMT in these cells.
conclusionsOur data demonstrate that miR-206 inhibits TGF-β transcription and autocrine production, as well as downstream target genes of EMT. Restoring miR-206 expression may provide an effective therapeutic strategy for ER positive BC.
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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.