ArticleCell communication and signaling : CCS2011
IGF-1 increases invasive potential of MCF 7 breast cancer cells and induces activation of latent TGF-β1 resulting in epithelial to mesenchymal transition.
Article in Cell communication and signaling : CCS, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 99 citations in OpenAlex.
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- Hypoxia-induced ELF3 promotes tumor angiogenesis through IGF1/IGF1R.EMBO reports · 2022Article
- miR-4286 is Involved in Connections Between IGF-1 and TGF-β Signaling for the Mesenchymal Transition and Invasion by Glioblastomas.Cellular and molecular neurobiology · 2022Article
- Circular RNA circPLK1 promotes breast cancer cell proliferation, migration and invasion by regulating miR-4500/IGF1 axis.Cancer cell international · 2020Article
- IGFBP-1 Expression Promotes Tamoxifen Resistance in Breast Cancer Cells via Erk Pathway Activation.Frontiers in endocrinology · 2020Article
- Microenvironmental Determinants of Breast Cancer Metastasis: Focus on the Crucial Interplay Between Estrogen and Insulin/Insulin-Like Growth Factor Signaling.Frontiers in cell and developmental biology · 2020Review
- The role of cellular contact and TGF-beta signaling in the activation of the epithelial mesenchymal transition (EMT).Cell adhesion & migration · 2019Article
- Modulation of RECK levels inJournal of biological research (Thessalonike, Greece) · 2019Article
- Non-target Genes Regulate miRNAs-Mediated Migration Steering of Colorectal Carcinoma.Pathology oncology research : POR · 2019Article
- Role of cellular reprogramming and epigenetic dysregulation in acquired chemoresistance in breast cancer.Cancer drug resistance (Alhambra, Calif.) · 2019Review
- An efficient method for bacterial production and activity assessment of recombinant human insulin like growth factor 1.Molecular biology reports · 2018Article
- Obesity-Activated Adipose-Derived Stromal Cells Promote Breast Cancer Growth and Invasion.Neoplasia (New York, N.Y.) · 2018Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionTGF-β signaling has been extensively studied in many developmental contexts, amongst which is its ability to induce epithelial to mesenchymal transitions (EMT). EMTs play crucial roles during embryonic development and have also come under intense scrutiny as a mechanism through which breast cancers progress to become metastatic. Interestingly, while the molecular hallmarks of EMT progression (loss of cell adhesion, nuclear localization of β-catenin) are straightforward, the cellular signaling cascades that result in an EMT are numerous and diverse. Furthermore, most studies describing the biological effects of TGF-β have been performed using high concentrations of active, soluble TGF-β, despite the fact that TGF-β is produced and secreted as a latent complex.
methodsMCF-7 breast cancer cells treated with recombinant IGF-1 were assayed for metalloproteinase activity and invasiveness through a matrigel coated transwell invasion chamber. IGF-1 treatments were then followed by the addition of latent-TGF-β1 to determine if elevated levels of IGF-1 together with latent-TGF-β1 could cause EMT.
resultsResults showed that IGF-1 - a molecule known to be elevated in breast cancer is a regulator of matrix metalloproteinase activity (MMP) and the invasive potential of MCF-7 breast cancer cells. The effects of IGF-1 appear to be mediated through signals transduced via the PI3K and MAPK pathways. In addition, increased IGF-1, together with latent TGF-β1 and active MMPs result in EMT.
conclusionsTaken together our data suggest a novel a link between IGF-1 levels, MMP activity, TGF-β signaling, and EMT in breast cancer cells.
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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.