ArticleCell journal2020
Repression of TGF-β Signaling in Breast Cancer Cells by miR-302/367 Cluster.
Article in Cell journal, 2020. 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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Who cites it
5 citing papers in PubMed.
- Enhancing Pluripotency and Adipogenic Differentiation in Human Adipose Tissue-Derived Stem Cells Through miR-302/367 Cluster Overexpression.Cellular and molecular bioengineering · 2025Article
- The miR-302s/367 Cluster Inhibits the Proliferation and Apoptosis in Sheep Fetal Fibroblasts via the Cell Cycle and PI3K-Akt Pathways.Mammalian genome : official journal of the International Mammalian Genome Society · 2021Article
- Drug Resistance in Metastatic Breast Cancer: Tumor Targeted Nanomedicine to the Rescue.International journal of molecular sciences · 2021Review
- miR-214-5p targeted by LncRNA DANCR mediates TGF-β signaling pathway to accelerate proliferation, migration and inhibit apoptosis of prostate cancer cells.American journal of translational research · 2021Article
- A Deep-Learning Model With the Attention Mechanism Could Rigorously Predict Survivals in Neuroblastoma.Frontiers in oncology · 2021Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveEpigenetic alterations of the malignantly transformed cells have increasingly been regarded as an important event in the carcinogenic development. Induction of some miRNAs such as miR-302/367 cluster has been shown to induce reprogramming of breast cancer cells and exert a tumor suppressive role by induction of mesenchymal to epithelial transition, apoptosis and a lower proliferation rate. Here, we aimed to investigate the impact of miR-302/367 overexpression on transforming growth factor-beta (TGF-β) signaling and how this may contribute to tumor suppressive effects of miR-302/367 cluster. MATERIALS AND
methodsIn this experimental study, MDA-MB-231 and SK-BR-3 breast cancer cells were cultured and transfected with miR-302/367 expressing lentivector. The impact of miR-302/367 overexpression on several mediators of TGF-β signaling and cell cycle was assessed by quantitative real-time polymerase chain reaction (qPCR) and flow cytometry.
resultsEctopic expression of miR-302/367 cluster downregulated expression of some downstream elements of TGF-β pathway in MDA-MB-231 and SK-BR-3 breast cancer cell lines. Overexpression of
conclusionTGF-β signaling is one of the key pathways in tumor progression and a general suppression of TGF-β mediators by the pleiotropically acting miR-302/367 cluster may be one of the important reasons for its anti-tumor effects in breast cancer cells.
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