Cadmium-induced Carcinogenesis in Respiratory Organs and the Prostate: Insights from Three Perspectives on Toxicogenomic Approach

Abstract

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.

Keywords: Adverse outcome pathways; Cadmium; Carcinogenesis; Computational biology; Toxicogenetics.

Figure 1. The route through which inhaled cadmium passes the respiratory organs and circulates in the bloodstream to reach the prostate.

Figure 2. Inclusive understanding about cadmium (Cd) exposure in respiratory organs.

(A) Comprehensive molecular network for the differentially expressed genes (DEGs) with cell process and diseases. (B) Condensed network containing hub genes. (C) Potential adverse outcome pathways (AOPs) for cadmium carcinogenicity in bronchial epithelium. KEGG, Kyoto Encyclopedia of Genes and Genomes; MIE, molecular initiating event; KE, key event; AO, adverse outcome.

Figure 3. Inclusive understanding about cadmium (Cd) occupational exposure in prostate.

(A) Comprehensive molecular network for the differentially expressed genes (DEGs) with cell process and diseases. (B) Condensed network containing hub genes. (C) Potential adverse outcome pathways (AOPs) for Cd carcinogenicity in prostate epithelium. KEGG, Kyoto Encyclopedia of Genes and Genomes; ROS, reactive oxygen species; MIE, molecular initiating event; KE, key event; AO, adverse outcome.