Abstract
Simple SummaryThe exposure of cancer cells to cadmium compounds may be associated with the acceleration of tumor progression. It is known that cadmium is a transcriptional regulator, and the study of differentially expressed genes has enabled the identification and classification of cadmium-associated molecular signatures as useful biomarkers that are potentially transferable to clinical research. This review recapitulates the studies that report the detection of such signatures in breast, gastric, colon, liver, lung, and nasopharyngeal tumor cell models, as specifically demonstrated by individual gene or whole genome expression profiling.The exposure of cancer cells to cadmium and its compounds is often associated with the development of more malignant phenotypes, thereby contributing to the acceleration of tumor progression. It is known that cadmium is a transcriptional regulator that induces molecular reprogramming, and therefore the study of differentially expressed genes has enabled the identification and classification of molecular signatures inherent in human neoplastic cells upon cadmium exposure as useful biomarkers that are potentially transferable to clinical research. This review recapitulates selected studies that report the detection of cadmium-associated signatures in breast, gastric, colon, liver, lung, and nasopharyngeal tumor cell models, as specifically demonstrated by individual gene or whole genome expression profiling. Where available, the molecular, biochemical, and/or physiological aspects associated with the targeted gene activation or silencing in the discussed cell models are also outlined.
Highlights
A Short Excursus on Cadmium and Eukaryotic Cell SystemsCadmium (Cd) is an underground mineral extracted as part of zinc deposits which, along with its compounds, exhibits a broad range of applications in the industry spanning from battery components to stabilizers for plastics, electroplated coatings for non-ferrous metals and dye pigments
The former was established from a pleural effusion of a triple-negative breast cancer (TNBC) of basal morphology, which was negative for estrogen receptor (ER) α and progesterone receptor (PR) expression and its p53 was inactivated by a mutation in codon 280 of exon 8
RH460 established after selection via the exposure of the parental line to increasing Cell SystemsCadmium (Cd) concentrations [92]; (ii) H1299 established from a lymph node metastasis of the lung from a patient who had received prior radiation therapy and endowed with a homozygous partial p53 deletion determining the lack of protein expression; and (iii) A549 characterized by mutant K-ras, wild-type EGFR and the properties of type II alveolar epithelial cells [93]
Summary
Cadmium (Cd) is an underground mineral extracted as part of zinc deposits which, along with its compounds, exhibits a broad range of applications in the industry spanning from battery components to stabilizers for plastics, electroplated coatings for non-ferrous metals and dye pigments. Reports in the literature have shown that mitochondria are one of the main intracellular targets for Cd toxicity due to the blocking of the electron transfer chain at complex III, which is considered the principal site for the production of reactive oxygen species (ROS), thereby favoring the over-production of the latter at the expense of ATP This leads to a dissipation of mitochondrial transmembrane potential with a consequent alteration of the cell’s redox status and mitochondrial and nuclear gene expression and the genome integrity [6,7]. As a further DNA-directed activity, evidence has been produced that Cd may be regarded as an epigenetic modulator, given its ability to alter the global DNA methylation pattern via the down-regulation of DNA methyltransferase activity and demethylation which, upon prolonged exposure, turns into enhanced enzyme activity and genome hypermethylation These opposite alterations may result in the up-regulation of cellular protooncogenes and the silencing of oncosuppressor genes, respectively [14,15]. The molecular, biochemical and/or physiological aspects associated with the targeted gene activation or silencing in the discussed cell models will be briefly outlined
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