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Platelet ATP, Thyroid Hormone Receptor on Integrin αvβ3 and Cancer Metastasis
Paul J Davis1,2,3, Shaker A Mousa4, Geraldine P Schechter5,6
1Department of Medicine, Albany Medical College, Albany, NY, USA. pdavis.ordwayst@gmail.com.
Hormones & Cancer
|December 16, 2019
Summary
Thyroid hormone (T4) acts as a pro-metastatic factor by activating integrin αvβ3 on tumor cells and platelets. This interaction promotes cancer cell invasion and metastasis through platelet degranulation and extracellular ATP release.
Area of Science:
- Oncology
- Endocrinology
- Cell Biology
Background:
- Platelets play a role in cancer metastasis by interacting with tumor cells.
- Integrins on cell and platelet surfaces mediate these crucial interactions.
- Thyroid hormone L-thyroxine (T4) is a key ligand for integrin αvβ3.
Purpose of the Study:
- To review the molecular mechanisms by which T4 influences cancer cell-platelet interactions.
- To elucidate the role of T4 as a pro-metastatic factor.
- To highlight the significance of integrin αvβ3 in thyroid hormone-mediated metastasis.
Main Methods:
- Review of existing literature on T4, integrins, platelets, and cancer metastasis.
- Analysis of molecular pathways involving integrin αvβ3 activation.
- Examination of extracellular ATP's role in tumor cell invasiveness.
Main Results:
- T4 activates integrin αvβ3 on both tumor cells and platelets.
- Activated integrins promote platelet aggregation and degranulation, releasing ATP.
- Extracellular ATP enhances tumor cell proliferation, invasiveness, and metastasis.
Conclusions:
- Thyroid hormone (T4) functions as a pro-metastatic factor.
- The T4-integrin αvβ3 axis is a critical mediator of cancer metastasis.
- Targeting this pathway may offer novel therapeutic strategies for cancer.
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