The Adipose Tissue at the Crosstalk Between EDCs and Cancer Development.
The Adipose Tissue at the Crosstalk Between EDCs and Cancer Development.
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DOI：
10.3389/fendo.2021.691658
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发表时间：
2021
影响因子：
5.2
通讯作者：
Chevalier N
中科院分区：
文献类型：
--
作者：
Bokobza E;Hinault C;Tiroille V;Clavel S;Bost F;Chevalier N
肥胖是一个主要的公共卫生问题，是包括癌症在内的许多疾病的根源。其中，胃肠道癌症的发病率显着升高，激素依赖性癌症也是如此。超重引起的代谢变化主要伴随着脂肪组织（AT）的发展、胰岛素抵抗和慢性炎症，导致荷尔蒙和/或生长因子失衡，从而影响细胞增殖和分化。 AT 现在被认为是内分泌干扰化学物质 (EDC) 的主要内部来源，代表了低水平的全身慢性暴露。有些 EDC 是不可代谢的，可以在 AT 中长期积累。我们长期接触低剂量的 EDC，这些 EDC 会干扰身体的内分泌代谢。重要的是，一些 EDC 参与了肥胖的发生，并深刻影响了 AT 的生理学。与此同时，EDC 与癌症的发展有关，特别是激素依赖性癌症（前列腺癌、睾丸癌、乳腺癌、子宫内膜癌、甲状腺癌）。虽然现在已经确定 AT 分泌促进肿瘤进展的脂肪细胞因子，但尚不清楚它们是否会引发癌症。因此，更好地了解 EDC 的作用，并使用建议揭示和验证人类这些机制的适当模型来研究 AT 在癌细胞进展和起始过程中的缓冲作用非常重要。我们将在这里回顾和论证 AT 作为 EDC 和激素依赖性癌症发展之间的串扰的潜在作用，以及如何评估它。
Obesity is a major public health concern at the origin of many pathologies, including cancers. Among them, the incidence of gastro-intestinal tract cancers is significantly increased, as well as the one of hormone-dependent cancers. The metabolic changes caused by overweight mainly with the development of adipose tissue (AT), insulin resistance and chronic inflammation induce hormonal and/or growth factor imbalances, which impact cell proliferation and differentiation. AT is now considered as the main internal source of endocrine disrupting chemicals (EDCs) representing a low level systemic chronic exposure. Some EDCs are non-metabolizable and can accumulate in AT for a long time. We are chronically exposed to low doses of EDCs able to interfere with the endocrine metabolism of the body. Importantly, several EDCs have been involved in the genesis of obesity affecting profoundly the physiology of AT. In parallel, EDCs have been implicated in the development of cancers, in particular hormone-dependent cancers (prostate, testis, breast, endometrium, thyroid). While it is now well established that AT secretes adipocytokines that promote tumor progression, it is less clear whether they can initiate cancer. Therefore, it is important to better understand the effects of EDCs, and to investigate the buffering effect of AT in the context of progression but also initiation of cancer cells using adequate models recommended to uncover and validate these mechanisms for humans. We will review and argument here the potential role of AT as a crosstalk between EDCs and hormone-dependent cancer development, and how to assess it.
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