ArticleHormones & cancer2017
Thyroid Hormone Controls Breast Cancer Cell Movement via Integrin αV/β3/SRC/FAK/PI3-Kinases.
Article in Hormones & cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 44 citations in OpenAlex.
- Association between Benign Thyroid Disorders and Breast Cancer Risk in Korean Women.Cancer research and treatment · 2026Article
- Exploring the molecular mechanisms of comorbidity between thyroid cancer and breast cancer through multi-omics data.Scientific reports · 2025Article
- Decoding the mechanisms behind second primary cancers.Journal of translational medicine · 2025Review
- COL12A1 Promotes Osteosarcoma Progression via the FAK/PI3K/AKT/mTOR Pathway.Current molecular medicine · 2025Article
- ERRα: unraveling its role as a key player in cell migration.Oncogene · 2024Review
- Sanguinarine inhibits melanoma invasion and migration by targeting the FAK/PI3K/AKT/mTOR signalling pathway.Pharmaceutical biology · 2023Article
- Daily exposure to low concentrations Tetrabromobisphenol A interferes with the thyroid hormone pathway in HepG2 cells.Fundamental research · 2023Article
- Links between Breast and Thyroid Cancer: Hormones, Genetic Susceptibility and Medical Interventions.Cancers · 2022Review
- Hormonal Crosstalk Between Thyroid and Breast Cancer.Endocrinology · 2022Review
- Integrin α3/α6 and αV are implicated in ADAM15-activated FAK and EGFR signalling pathway individually and promote non-small-cell lung cancer progression.Cell death & disease · 2022Article
- The TSH/Thyroid Hormones Axis and Breast Cancer.Journal of clinical medicine · 2022Review
- Thyroid Diseases and Breast Cancer.Journal of personalized medicine · 2022Review
- Role of thyroid hormone-integrin αvβ3-signal and therapeutic strategies in colorectal cancers.Journal of biomedical science · 2021Review
- Understanding the role of integrins in breast cancer invasion, metastasis, angiogenesis, and drug resistance.Oncogene · 2021Review
- Thyroxine Induces Acute Relaxation of Rat Skeletal Muscle Arteries via Integrin αvβ3, ERK1/2 and Integrin-Linked Kinase.Frontiers in physiology · 2021Article
- Extracellular Matrix: Emerging Roles and Potential Therapeutic Targets for Breast Cancer.Frontiers in oncology · 2021Review
- Impact of Hypothyroidism on Patients with Hepatocellular Carcinoma Undergoing Liver Transplantation.International journal of general medicine · 2021Article
- Hyperthyroidism is associated with breast cancer risk and mammographic and genetic risk predictors.BMC medicine · 2020Article
- Decreased expression of the thyroid hormone-inactivating enzyme type 3 deiodinase is associated with lower survival rates in breast cancer.Scientific reports · 2020Article
- Extracellular Matrix Derived from High Metastatic Human Breast Cancer Triggers Epithelial-Mesenchymal Transition in Epithelial Breast Cancer Cells through αvβ3 Integrin.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thyroid hormones (TH) play a fundamental role in diverse processes, including cellular movement. Cell migration requires the integration of events that induce changes in cell structure towards the direction of migration. These actions are driven by actin remodeling and stabilized by the development of adhesion sites to extracellular matrix via transmembrane receptors linked to the actin cytoskeleton. Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that promotes cell migration and invasion through the control of focal adhesion turnover. In this work, we demonstrate that the thyroid hormone triiodothyronine (T3) regulates actin remodeling and cell movement in breast cancer T-47D cells through the recruitment of FAK. T3 controls FAK phosphorylation and translocation at sites where focal adhesion complexes are assembled. This process is triggered via rapid signaling to integrin αV/β3, Src, phosphatidylinositol 3-OH kinase (PI3K), and FAK. In addition, we established a cellular model with different concentration of T3 levels: normal, absence, and excess in T-47D breast cancer cells. We found that the expression of Src, FAK, and PI3K remained at normal levels in the excess of T3 model, while it was significantly reduced in the absence model. In conclusion, these results suggest a novel role for T3 as an important modulator of cell migration, providing a starting point for the development of new therapeutic strategies for breast cancer treatment.
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