A review of molecular events of cadmium-induced carcinogenesis.
A review of molecular events of cadmium-induced carcinogenesis.
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DOI：
10.1615/jenvironpatholtoxicoloncol.2014011075
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发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Damodaran C
中科院分区：
文献类型：
--
作者：
Luevano J;Damodaran C
镉（Cd）是一种有毒的重工业金属，对人类和野生动物造成严重的环境健康危害。最近，镉和含镉化合物已被列为已知的人类致癌物和流行病学数据显示与前列腺癌，乳腺癌和肺癌的因果关系。镉诱导的致癌作用的分子机制知之甚少，现在才开始被阐明。近年来，由于镉致动物恶性肿瘤的发生，镉的慢性暴露效应引起了人们极大的兴趣。简而言之，各种体外研究表明，镉可以作为有丝分裂原，刺激细胞增殖，抑制细胞凋亡和DNA修复，并诱导几种哺乳动物组织和器官的致癌作用。因此，慢性镉暴露和恶性转化的各种机制需要进一步研究。在这篇综述中，我们将集中在最近的证据，各种领先的一般和组织特异性的分子机制，以下慢性暴露于镉在前列腺，乳腺癌和肺转化的恶性肿瘤。此外，这篇综述考虑了不太明确的机制，如表观遗传修饰和自噬，这被认为是发挥了作用，在镉诱导的恶性转化的发展。
Cadmium (Cd) is a toxic, heavy industrial metal that poses serious environmental health hazards to both humans and wildlife. Lately, Cd and Cd containing compounds have been classified as known human carcinogens and epidemiological data show causal associations with prostate, breast and lung cancer. The molecular mechanisms involved in Cd-induced carcinogenesis are poorly understood and are only now beginning to be elucidated. The effects of chronic exposure to Cd have recently become of great interest due to the development of malignancies in Cd-induced tumorigenesis in animal. Briefly, various in vitro studies demonstrate that Cd can act as a mitogen, stimulate cell proliferation, inhibit apoptosis and DNA repair, and induce carcinogenesis in several mammalian tissues and organs. Thus, the various mechanisms involved in chronic Cd exposure and malignant transformations warrant further investigation. In this review, we will focus on recent evidence of various leading general and tissue specific molecular mechanisms that follow chronic exposure to Cd in prostate, breast and lung transformed malignancies. In addition, this review considers less defined mechanisms such as epigenetic modification and autophagy, which are thought to play a role in the development of Cd-induced malignant transformation.
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