Thyroid hormones and their membrane receptors as therapeutic targets for T cell lymphomas
Thyroid hormones (THs) are important regulators of metabolism, differentiation and cell proliferation. They can modify the physiology of human and murine T cell lymphomas (TCL). These effects involve genomic mechanisms, mediated by specific nuclear receptors (TR), as well as nongenomic mechanisms, t...
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todo:paper_10436618_v109_n_p55_Cremaschi2023-10-03T15:58:13Z Thyroid hormones and their membrane receptors as therapeutic targets for T cell lymphomas Cremaschi, G.A. Cayrol, F. Sterle, H.A. Díaz Flaqué, M.C. Barreiro Arcos, M.L. Angiogenesis Integrin αvβ3 Proliferation T cell lymphoma Thyroid hormones cilengitide liothyronine thyroid hormone thyroid hormone receptor thyrotropin thyroxine vasculotropin vitronectin receptor thyroid hormone thyroid hormone receptor cancer recurrence CD8+ T lymphocyte drug targeting glioblastoma human hyperthyroidism hypothyroidism metastasis natural killer cell nonhuman priority journal Review solid tumor T cell lymphoma T-Cell lymphoma cell line tumor escape tumor growth tumor microenvironment tumor vascularization animal genetics genomics Lymphoma, T-Cell metabolism T lymphocyte Animals Genomics Humans Lymphoma, T-Cell Receptors, Thyroid Hormone T-Lymphocytes Thyroid Hormones Thyroid hormones (THs) are important regulators of metabolism, differentiation and cell proliferation. They can modify the physiology of human and murine T cell lymphomas (TCL). These effects involve genomic mechanisms, mediated by specific nuclear receptors (TR), as well as nongenomic mechanisms, that lead to the activation of different signaling pathways through the activation of a membrane receptor, the integrin αvβ3. Therefore, THs are able to induce the survival and growth of TCL. Specifically, the signaling induced by THs through the integrin αvβ3 activates proliferative and angiogenic programs, mediated by the regulation of the vascular endothelial growth factor (VEGF). The genomic or pharmacologic inhibition of integrin αvβ3 reduces the production of VEGF and induces cell death both in vitro and in xenograft models of human TCL. Here we review the mechanisms involved in the modulation of the physiology of TCL induced by THs, the analysis of the interaction between genomic and nongenomic actions of THs and their contribution to T cell lymphomagenesis. These actions of THs suggest a novel mechanism for the endocrine modulation of the physiopathology of TCL and they provide a potential molecular target for its treatment. © 2016 Elsevier Ltd. Fil:Barreiro Arcos, M.L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_10436618_v109_n_p55_Cremaschi |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
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R-134 |
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Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
Angiogenesis Integrin αvβ3 Proliferation T cell lymphoma Thyroid hormones cilengitide liothyronine thyroid hormone thyroid hormone receptor thyrotropin thyroxine vasculotropin vitronectin receptor thyroid hormone thyroid hormone receptor cancer recurrence CD8+ T lymphocyte drug targeting glioblastoma human hyperthyroidism hypothyroidism metastasis natural killer cell nonhuman priority journal Review solid tumor T cell lymphoma T-Cell lymphoma cell line tumor escape tumor growth tumor microenvironment tumor vascularization animal genetics genomics Lymphoma, T-Cell metabolism T lymphocyte Animals Genomics Humans Lymphoma, T-Cell Receptors, Thyroid Hormone T-Lymphocytes Thyroid Hormones |
| spellingShingle |
Angiogenesis Integrin αvβ3 Proliferation T cell lymphoma Thyroid hormones cilengitide liothyronine thyroid hormone thyroid hormone receptor thyrotropin thyroxine vasculotropin vitronectin receptor thyroid hormone thyroid hormone receptor cancer recurrence CD8+ T lymphocyte drug targeting glioblastoma human hyperthyroidism hypothyroidism metastasis natural killer cell nonhuman priority journal Review solid tumor T cell lymphoma T-Cell lymphoma cell line tumor escape tumor growth tumor microenvironment tumor vascularization animal genetics genomics Lymphoma, T-Cell metabolism T lymphocyte Animals Genomics Humans Lymphoma, T-Cell Receptors, Thyroid Hormone T-Lymphocytes Thyroid Hormones Cremaschi, G.A. Cayrol, F. Sterle, H.A. Díaz Flaqué, M.C. Barreiro Arcos, M.L. Thyroid hormones and their membrane receptors as therapeutic targets for T cell lymphomas |
| topic_facet |
Angiogenesis Integrin αvβ3 Proliferation T cell lymphoma Thyroid hormones cilengitide liothyronine thyroid hormone thyroid hormone receptor thyrotropin thyroxine vasculotropin vitronectin receptor thyroid hormone thyroid hormone receptor cancer recurrence CD8+ T lymphocyte drug targeting glioblastoma human hyperthyroidism hypothyroidism metastasis natural killer cell nonhuman priority journal Review solid tumor T cell lymphoma T-Cell lymphoma cell line tumor escape tumor growth tumor microenvironment tumor vascularization animal genetics genomics Lymphoma, T-Cell metabolism T lymphocyte Animals Genomics Humans Lymphoma, T-Cell Receptors, Thyroid Hormone T-Lymphocytes Thyroid Hormones |
| description |
Thyroid hormones (THs) are important regulators of metabolism, differentiation and cell proliferation. They can modify the physiology of human and murine T cell lymphomas (TCL). These effects involve genomic mechanisms, mediated by specific nuclear receptors (TR), as well as nongenomic mechanisms, that lead to the activation of different signaling pathways through the activation of a membrane receptor, the integrin αvβ3. Therefore, THs are able to induce the survival and growth of TCL. Specifically, the signaling induced by THs through the integrin αvβ3 activates proliferative and angiogenic programs, mediated by the regulation of the vascular endothelial growth factor (VEGF). The genomic or pharmacologic inhibition of integrin αvβ3 reduces the production of VEGF and induces cell death both in vitro and in xenograft models of human TCL. Here we review the mechanisms involved in the modulation of the physiology of TCL induced by THs, the analysis of the interaction between genomic and nongenomic actions of THs and their contribution to T cell lymphomagenesis. These actions of THs suggest a novel mechanism for the endocrine modulation of the physiopathology of TCL and they provide a potential molecular target for its treatment. © 2016 Elsevier Ltd. |
| format |
JOUR |
| author |
Cremaschi, G.A. Cayrol, F. Sterle, H.A. Díaz Flaqué, M.C. Barreiro Arcos, M.L. |
| author_facet |
Cremaschi, G.A. Cayrol, F. Sterle, H.A. Díaz Flaqué, M.C. Barreiro Arcos, M.L. |
| author_sort |
Cremaschi, G.A. |
| title |
Thyroid hormones and their membrane receptors as therapeutic targets for T cell lymphomas |
| title_short |
Thyroid hormones and their membrane receptors as therapeutic targets for T cell lymphomas |
| title_full |
Thyroid hormones and their membrane receptors as therapeutic targets for T cell lymphomas |
| title_fullStr |
Thyroid hormones and their membrane receptors as therapeutic targets for T cell lymphomas |
| title_full_unstemmed |
Thyroid hormones and their membrane receptors as therapeutic targets for T cell lymphomas |
| title_sort |
thyroid hormones and their membrane receptors as therapeutic targets for t cell lymphomas |
| url |
http://hdl.handle.net/20.500.12110/paper_10436618_v109_n_p55_Cremaschi |
| work_keys_str_mv |
AT cremaschiga thyroidhormonesandtheirmembranereceptorsastherapeutictargetsfortcelllymphomas AT cayrolf thyroidhormonesandtheirmembranereceptorsastherapeutictargetsfortcelllymphomas AT sterleha thyroidhormonesandtheirmembranereceptorsastherapeutictargetsfortcelllymphomas AT diazflaquemc thyroidhormonesandtheirmembranereceptorsastherapeutictargetsfortcelllymphomas AT barreiroarcosml thyroidhormonesandtheirmembranereceptorsastherapeutictargetsfortcelllymphomas |
| _version_ |
1807323720275984384 |