Arsenic and cancer: Evidence and mechanisms

Speer, Rachel M.; Zhou, Xixi; Volk, Lindsay; Liu, Ke Jian; Hudson, Laurie G.

doi:10.1016/bs.apha.2022.08.001

Cited by 12 publications

(3 citation statements)

References 270 publications

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“…TPA, a strong tumor promoter, is essential for initiating a number of cellular processes that lead to the development of cancer. Arsenic, a natural element and environmental pollutant, has been linked to several types of cancer and has subtle, long-term effects on cellular DNA integrity [56]. Topoisomerase inhibitors hinder DNA replication and repair processes, leading to the accumulation of genetic mutations.…”

Section: Types Of Carcinogensmentioning

confidence: 99%

Cancer Initiation and Progression: A Comprehensive Review of Carcinogenic Substances, Anti-Cancer Therapies, and Regulatory Frameworks

Bhat,

Ahmed,

Abbas

et al. 2024

Asian J. Res. Biochem.

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Cancer is a multifaceted disease influenced by genetic mutations and environmental factors, including exposure to carcinogens. This review presents an in-depth analysis of the mechanisms driving cancer initiation, focusing on the roles of carcinogenic chemicals, anticancer therapies, and chemo-preventive agents. The discussion encompasses a broad spectrum of carcinogens: chemical agents like polycyclic aromatic hydrocarbons, physical agents such as ionizing radiation, biological agents like viruses, and certain therapeutic drugs. The multistep nature of carcinogenesis—comprising initiation, promotion, and progression phases—is detailed, with an emphasis on genetic and epigenetic alterations. Methods for testing carcinogenicity, including in vitro and in vivo studies and epidemiological approaches, are highlighted for their significance in identifying potential carcinogens and understanding their mechanisms. To classify and regulate carcinogenic exposures, the review also looks at the risk management plans and regulatory frameworks used by agencies like the European Chemicals Agency (ECHA), the Environmental Protection Agency (EPA), and the International Agency for Research on Cancer (IARC). Additionally, emerging trends in cancer treatment, such as precision oncology, immunotherapy, and early detection technologies, are explored, alongside ongoing challenges like health disparities and ethical issues. The review emphasizes the necessity of a multidisciplinary approach, involving collaboration among researchers, clinicians, regulatory bodies, and public health organizations, to translate scientific findings into effective cancer prevention, detection, and treatment strategies.

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Section: Types Of Carcinogensmentioning

confidence: 99%

Cancer Initiation and Progression: A Comprehensive Review of Carcinogenic Substances, Anti-Cancer Therapies, and Regulatory Frameworks

Bhat,

Ahmed,

Abbas

et al. 2024

Asian J. Res. Biochem.

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“…It is estimated that approximately 200 million people around the world are exposed to unsafe levels of arsenic (Podgorski and Berg 2020). Chronic arsenic exposure has been correlated with many types of cancer (e.g., lung, liver, bladder, kidneys, skin, prostate), as well as non-carcinogenic diseases such as skin lesions, cardiovascular disease, reproductive defects, neurological injuries, and diabetes mellitus (Chen et al 2019; Benbrahim-Tallaa and Waalkes 2008; Speer et al 2023). Several studies indicated that long-term exposure to arsenic increases the risk of prostate cancer morbidity and mortality (Garcia-Esquinas et al…”

Section: Introductionmentioning

confidence: 99%

Chronic NaAsO2 exposure promotes migration and invasion of prostate cancer cells by Akt/GSK-3β/β-catenin/TCF4 axis-mediated epithelial-mesenchymal transition

Zhang,

Yan,

Liu

et al. 2024

Preprint

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Inorganic arsenic is a Class I human Carcinogen. However, the role of chronic inorganic arsenic exposure on prostate cancer metastasis still unclear. This study aimed to investigate the effect and mechanism of chronic NaAsO2 exposure on migration and invasion of prostate cancer cells. DU145 and PC-3 cells were exposed to NaAsO2 (2 µmol/L) for 25 generations. Wound healing and Transwell assays showed that chronic NaAsO2 exposure promoted migration and invasion of DU145 and PC-3 cells. In addition, chronic NaAsO2 exposure induced epithelial-mesenchymal transition (EMT) of DU145 cells by promoting β-catenin/TCF4 transcriptional activity. Mechanically, NaAsO2 promoted GSK-3β inactivation in the "disruption complex" through Akt mediated phosphorylation at serine 9, and then inhibited phosphorylation and ubiquitination degradation of β-catenin, leading to β-catenin nuclear translocation. Ly204002, a selective phosphatidylinositol 3-kinase (PI3K)/Akt inhibitor, suppressed the β-catenin/TCF4 complex activation and EMT through blocking the Akt-mediated GSK-3β inactivation in the "disruption complex" in chronic NaAsO2 exposed DU145 and PC-3 cells. Moreover, Ly204002 alleviated chronic NaAsO2-induced migration and invasion in DU145 and PC-3 cells. These findings provide evidence that chronic arsenic exposure promoted migration and invasion of prostate cancer cells through inducing EMT driven by AKT/GSK-3β/β-catenin/TCF4 signaling axis. Akt is expected to be a potential therapeutic target for chronic arsenic exposure-mediated prostate cancer metastasis.

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“…As generates reactive oxygen species that cause oxidative stress, leading to DNA damage. Concurrently, As inhibits DNA repair, modifies the epigenetic regulation of gene expression, and targets protein function due to its ability to replace zinc in select proteins [ 31 ]. In a recent study, we have shown that high As exposure was associated with impaired DNA replication pathways, cellular response to different DNA damage repair mechanisms, and immune response [ 32 ].…”

Section: Introductionmentioning

confidence: 99%

Molecular Profiling and the Interaction of Somatic Mutations with Transcriptomic Profiles in Non-Melanoma Skin Cancer (NMSC) in a Population Exposed to Arsenic

Jasmine,

Argos,

Khamkevych

et al. 2024

Cells

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Exposure to inorganic arsenic (As) is recognized as a risk factor for non-melanoma skin cancer (NMSC). We followed up with 7000 adults for 6 years who were exposed to As. During follow-up, 2.2% of the males and 1.3% of the females developed basal cell carcinoma (BCC), while 0.4% of the male and 0.2% of the female participants developed squamous cell carcinoma (SCC). Using a panel of more than 400 cancer-related genes, we detected somatic mutations (SMs) in the first 32 NMSC samples (BCC = 26 and SCC = 6) by comparing paired (tissue–blood) samples from the same individual and then comparing them to the SM in healthy skin tissue from 16 participants. We identified (a) a list of NMSC-associated SMs, (b) SMs present in both NMSC and healthy skin, and (c) SMs found only in healthy skin. We also demonstrate that the presence of non-synonymous SMs in the top mutated genes (like PTCH1, NOTCH1, SYNE1, PKHD1 in BCC and TP53 in SCC) significantly affects the magnitude of differential expressions of major genes and gene pathways (basal cell carcinoma pathways, NOTCH signaling, IL-17 signaling, p53 signaling, Wnt signaling pathway). These findings may help select groups of patients for targeted therapy, like hedgehog signaling inhibitors, IL17 inhibitors, etc., in the future.

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Arsenic and cancer: Evidence and mechanisms

Cited by 12 publications

References 270 publications

Cancer Initiation and Progression: A Comprehensive Review of Carcinogenic Substances, Anti-Cancer Therapies, and Regulatory Frameworks

Cancer Initiation and Progression: A Comprehensive Review of Carcinogenic Substances, Anti-Cancer Therapies, and Regulatory Frameworks

Chronic NaAsO2 exposure promotes migration and invasion of prostate cancer cells by Akt/GSK-3β/β-catenin/TCF4 axis-mediated epithelial-mesenchymal transition

Molecular Profiling and the Interaction of Somatic Mutations with Transcriptomic Profiles in Non-Melanoma Skin Cancer (NMSC) in a Population Exposed to Arsenic

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