Actions of L-thyroxine (T4) and Tetraiodothyroacetic Acid (Tetrac) on Gene Expression in Thyroid Cancer Cells.

摘要: The clinical behavior of thyroid cancers is seen to reflect inherent transcriptional activities mutated genes and trophic effects on tumors circulating pituitary thyrotropin (TSH). hormone, L-thyroxine (T4), has been shown stimulate proliferation a large number different forms cancer. This activity T4 mediated by cell surface receptor the extracellular domain integrin αvβ3. In this brief review, we describe what known about as factor for differentiated (papillary follicular) cancers. Given T4′s cancer-stimulating in cancers, it was not surprising find that genomic actions were anti-apoptotic. Transduction T4-generated signal at primarily involved mitogen-activated protein kinase (MAPK). C cell-origin medullary carcinoma (MTC), hormone analogues, such tetraiodothyroacetic acid (tetrac), include pro-angiogenic apoptosis-linked genes. Tetrac an inhibitor αvβ3, assumed, but yet proved, anti-angiogenic pro-apoptotic tetrac MTC cells are matched We also note papillary may express leptin receptor, from adipocytes tumor proliferation. Transcription stimulated anaplastic, papillary, follicular carcinomas invasion, matrix metalloproteinases (MMPs). summary, analogues act their αvβ3 variety types cancer modulate transcription relevant invasiveness, apoptosis, angiogenesis. These independent TSH.