Department of Urology, University of Louisville, Louisville, KY, United States.
Department of Urology, University of Louisville, Louisville, KY, United States; College of Pharmacy, Department of Pharmaceutical Sciences, Texas A&M, College Station, TX, United States.
Semin Cancer Biol. 2021 Nov;76:247-257. doi: 10.1016/j.semcancer.2021.03.022. Epub 2021 Mar 30.
Environmental and/or occupational exposure to metals such as Arsenic (As), Cadmium (Cd), and Chromium (Cr) have been shown to induce carcinogenesis in various organs, including the urogenital system. However, the mechanisms responsible for metal-induced carcinogenesis remain elusive. We and others have shown that metals are potent inducers of autophagy, which has been suggested to be an adaptive stress response to allow metal-exposed cells to survive in hostile environments. Albeit few, recent experimental studies have shown that As and Cd promote tumorigenesis via autophagy and that inhibition of autophagic signaling suppressed metal-induced carcinogenesis. In light of the newly emerging role of autophagic involvement in metal-induced carcinogenesis, the present review focuses explicitly on the mechanistic role of autophagy and potential signaling pathways involved in As-, Cd-, and Cr-induced urogenital carcinogenesis.
环境和/或职业暴露于砷（As）、镉（Cd）和铬（Cr）等金属已被证明可在包括泌尿生殖系统在内的各种器官中诱导致癌作用。然而，导致金属诱导致癌作用的机制仍不清楚。我们和其他人已经表明，金属是自噬的有效诱导剂，自噬被认为是一种适应性应激反应，以使暴露于金属的细胞能够在恶劣环境中存活。尽管很少，但最近的实验研究表明，As 和 Cd 通过自噬促进肿瘤发生，并且抑制自噬信号抑制了金属诱导的致癌作用。鉴于自噬参与金属诱导的致癌作用的新出现作用，本综述专门重点介绍自噬在 As、Cd 和 Cr 诱导的泌尿生殖系统致癌作用中的机制作用以及涉及的潜在信号通路。
