镉诱导的呼吸器官和前列腺癌发病:从毒物基因组学方法的三个角度看问题。

IF 2.5 Q3 ONCOLOGY
Jun Lee, Dong Yeop Shin, Yujin Jang, Jun Pyo Han, Eun-Min Cho, Young Rok Seo
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引用次数: 0

摘要

镉(Cd)主要通过吸烟或职业暴露于受污染的空气中吸入。吸入镉后,镉最终会通过血液到达前列腺。在这篇综述中,我们研究了镉在呼吸器官和前列腺中的致癌潜力。具体来说,本综述通过探索基因本体、生物网络和不良后果途径,研究了细胞代谢、综合毒性和致癌机制。在呼吸器官中,镉通过改变 IL1B 和 FGF2 的表达、造成 DNA 损伤、降低细胞连接完整性和促进细胞凋亡诱发肺癌。在前列腺中,镉通过改变 EDN1 和 HMOX1 的表达,导致蛋白质活性和成熟异常,抑制肿瘤抑制因子,诱导细胞凋亡,从而诱发前列腺癌。总之,本综述通过采用毒物基因组学方法,对镉在两个不同器官中的致癌机制进行了全面的了解。这些见解可作为进一步研究镉诱发癌症的基础,有助于建立未来的癌症预防策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cadmium-induced Carcinogenesis in Respiratory Organs and the Prostate: Insights from Three Perspectives on Toxicogenomic Approach.

Cadmium (Cd) exposure primarily occurs through inhalation, either by smoking or occupational exposure to contaminated air. Upon inhalation, Cd ultimately reaches the prostate through the bloodstream. In this review, we investigate the carcinogenic potential of Cd in both respiratory organs and the prostate. Specifically, this review examines cellular metabolism, comprehensive toxicity, and carcinogenic mechanisms by exploring gene ontology, biological networks, and adverse outcome pathways. In the respiratory organs, Cd induces lung cancer by altering the expression of IL1B and FGF2, causing DNA damage, reducing cell junction integrity, and promoting apoptosis. In the prostate, Cd induces prostate cancer by modifying the expression of EDN1 and HMOX1, leading to abnormal protein activities and maturation, suppressing tumor suppressors, and inducing apoptosis. Collectively, this review provides a comprehensive understanding of the carcinogenic mechanisms of Cd in two different organs by adopting toxicogenomic approaches. These insights can serve as a foundation for further research on cadmium-induced cancer, contributing to the establishment of future cancer prevention strategies.

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