Lee Jun, Shin Dong Yeop, Jang Yujin, Han Jun Pyo, Cho Eun-Min, Seo Young Rok
Department of Life Science, Institute of Environmental Medicine for Green Chemistry, Dongguk University Biomedi Campus, Goyang, Korea.
Department of Nano, Chemical & Biological Engineering, College of Natural Science and Engineering, Seokyeong University, Seoul, Korea.
J Cancer Prev. 2023 Dec 30;28(4):150-159. doi: 10.15430/JCP.2023.28.4.150.
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 and , causing DNA damage, reducing cell junction integrity, and promoting apoptosis. In the prostate, Cd induces prostate cancer by modifying the expression of and , 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.
镉（Cd）暴露主要通过吸入发生，要么是吸烟，要么是职业性接触受污染空气。吸入后，镉最终通过血液循环到达前列腺。在本综述中，我们研究了镉在呼吸器官和前列腺中的致癌潜力。具体而言，本综述通过探索基因本体论、生物网络和不良结局途径，研究细胞代谢、综合毒性和致癌机制。在呼吸器官中，镉通过改变[具体基因1]和[具体基因2]的表达诱导肺癌，导致DNA损伤，降低细胞连接完整性，并促进细胞凋亡。在前列腺中，镉通过改变[具体基因3]和[具体基因4]的表达诱导前列腺癌，导致蛋白质活性和成熟异常，抑制肿瘤抑制因子，并诱导细胞凋亡。总体而言，本综述通过采用毒理基因组学方法，全面了解了镉在两个不同器官中的致癌机制。这些见解可为进一步研究镉诱导的癌症奠定基础，有助于制定未来的癌症预防策略。
