Thyroid cancer is the most common sort of endocrine-related cancer with more prevalent in women and elderly individuals which has quickly widespread expansion in worldwide over the recent decades. Common features of malignant thyroid cells are to have accelerated metabolism and increased glucose uptake to optimize their energy supply which provides a fundamental advantage for growth. In tumor cells the retaining of required energy charge for cell survival is imperative, indeed glucose transporters are enable of promoting of this task. According to this relation it has been reported the upregulation of glucose transporters in various types of cancers. Human studies indicated that poor survival can be occurred following the high levels of GLUT1 expression in tumors. GLUT-1 and GLUT3 are the glucose transporters which seems to be mainly engaged with the oncogenesis of thyroid cancer and their expression in malignant tissues is much more than in the normal one. They are promising targets for the advancement of anticancer strategies. The lack of oncosuppressors have dominant effect on the membrane expression of GLUT1 and glucose uptake. Overexpression of hypoxia inducible factors have been additionally connected with distant metastasis in thyroid cancers which mediates transcriptional regulation of glycolytic genes including GLUT1 and GLUT3. Though the physiological role of the thyroid gland is well illustrated, but the metabolic regulations in thyroid cancer remain evasive. In this study we discuss proliferation pathways of the key regulators and signaling molecules such as PI3K-Akt, HIF-1, MicroRNA, PTEN, AMPK, BRAF, c-Myc, TSH, Iodide and p53 which includes in the regulation of GLUTs in thyroid cancer cells. Incidence of deregulations in cellular energetics and metabolism are the most serious signs of cancers. In conclusion, understanding the mechanisms of glucose transportation in normal and pathologic thyroid tissues is critically important and could provide significant insights in science of diagnosis and treatment of thyroid disease.

中文翻译：

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甲状腺癌细胞系中葡萄糖摄取的调节剂。

甲状腺癌是最常见的内分泌相关癌症，在女性和老年人中更为普遍，近几十年来在全球范围内迅速蔓延。恶性甲状腺细胞的共同特征是加速新陈代谢和增加葡萄糖摄取以优化其能量供应，这为生长提供了基本优势。在肿瘤细胞中，必须保留细胞存活所需的能量电荷，实际上葡萄糖转运蛋白能够促进这项任务。根据这种关系，据报道在各种类型的癌症中葡萄糖转运蛋白的上调。人体研究表明，在肿瘤中 GLUT1 高水平表达后，可能会出现较差的存活率。GLUT-1和GLUT3是似乎主要参与甲状腺癌发生的葡萄糖转运蛋白，它们在恶性组织中的表达量远高于正常组织。它们是推进抗癌策略的有希望的目标。肿瘤抑制因子的缺乏对 GLUT1 的膜表达和葡萄糖摄取具有显着影响。缺氧诱导因子的过度表达还与甲状腺癌的远处转移有关，后者介导糖酵解基因（包括 GLUT1 和 GLUT3）的转录调控。虽然甲状腺的生理作用已得到很好的说明，但甲状腺癌的代谢调节仍然难以捉摸。在这项研究中，我们讨论了关键调节因子和信号分子的增殖途径，例如 PI3K-Akt、HIF-1、MicroRNA、PTEN、AMPK、BRAF、c-Myc、TSH、碘化物和 p53，包括调节甲状腺癌细胞中的 GLUT。细胞能量学和新陈代谢失调的发生率是癌症最严重的迹象。总之，了解正常和病理甲状腺组织中葡萄糖转运的机制至关重要，可以为甲状腺疾病的诊断和治疗科学提供重要的见解。