Quantitative and immunohistochemical evaluation of PCNA, androgen receptors, apoptosis, and Glutathione-S-Transferase P1 on preneoplastic changes induced by cadmium and zinc chloride in the rat ventral prostate

Arriazu, Riánsares; Pozuelo, José Manuel; Martı́n, Rocı́o; Rodríguez, Rosario; Santamarı́a, Luis

doi:10.1002/pros.20192

Cited by 24 publications

(26 citation statements)

References 43 publications

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“…In agreement with other reports [37][38][39][40][41][42][43], we found that GSTp was a reliable marker of basal cells in benign acini. This is similar to the distribution of CuZn-superoxide dismutase, another free radical scavenger [44,45].…”

Section: Discussionsupporting

confidence: 95%

Glutathione S-transferase: differential expression of α, μ, and π isoenzymes in benign prostate, prostatic intraepithelial neoplasia, and prostatic adenocarcinoma

2007

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Section: Discussionsupporting

confidence: 95%

Glutathione S-transferase: differential expression of α, μ, and π isoenzymes in benign prostate, prostatic intraepithelial neoplasia, and prostatic adenocarcinoma

2007

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“…The increased cell growth and expression of the cell proliferation marker gene PCNA and the cell cycle gene CyclinD1 in cells treated with cadmium suggest that cadmium has mitogenic potential. Although there are several reports on increased cell proliferation from cadmium exposure 31,32, there are very few reports on increased expression of PCNA and CyclinD1 in cadmium-exposed cells33,34.…”

Section: Discussionmentioning

confidence: 99%

Cadmium Induced Cell Apoptosis, DNA Damage, Decreased DNA Repair Capacity, and Genomic Instability during Malignant Transformation of Human Bronchial Epithelial Cells

Zhang¹,

Wang²,

Liu³

et al. 2013

Int. J. Med. Sci.

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Cadmium and its compounds are well-known human carcinogens, but the mechanisms underlying the carcinogenesis are not entirely understood. Our study was designed to elucidate the mechanisms of DNA damage in cadmium-induced malignant transformation of human bronchial epithelial cells. We analyzed cell cycle, apoptosis, DNA damage, gene expression, genomic instability, and the sequence of exons in DNA repair genes in several kinds of cells. These cells consisted of untreated control cells, cells in the fifth, 15th, and 35th passage of cadmium-treated cells, and tumorigenic cells from nude mice using flow cytometry, Hoechst 33258 staining, comet assay, quantitative real-time polymerase chain reaction (PCR), Western blot analysis, random amplified polymorphic DNA (RAPD)-PCR, and sequence analysis. We observed a progressive increase in cell population of the G0/G1 phase of the cell cycle and the rate of apoptosis, DNA damage, and cadmium-induced apoptotic morphological changes in cerebral cortical neurons during malignant transformation. Gene expression analysis revealed increased expression of cell proliferation (PCNA), cell cycle (CyclinD1), pro-apoptotic activity (Bax), and DNA damage of the checkpoint genes ATM, ATR, Chk1, Chk2, Cdc25A. Decreased expression of the anti-apoptotic gene Bcl-2 and the DNA repair genes hMSH2, hMLH1, ERCC1, ERCC2, and hOGG1 was observed. RAPD-PCR revealed genomic instability in cadmium-exposed cells, and sequence analysis showed mutation of exons in hMSH2, ERCC1, XRCC1, and hOGG1 in tumorigenic cells. This study suggests that Cadmium can increase cell apoptosis and DNA damage, decrease DNA repair capacity, and cause mutations, and genomic instability leading to malignant transformation. This process could be a viable mechanism for cadmium-induced cancers.

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“…Furthermore, DPI was shown to reduce cell proliferation in prostate cancer cells, including LNCaP cells which express the mutated AR protein and are dependent on AR for growth, but respond to other steroids than androgens and can be driven to a castration-resistant phenotype. In addition to oxidative stress induced by H 2 O 2 , cadmium and zinc chloride, which are known to induce oxidative stress, were reported to increase AR expression in dysplastic glands of rat prostate (Arriazu et al 2005). The synthetic antimicrobial chemical mequindox was found to induce oxidative stress and AR overexpression in rat testes, indicating a positive connection between oxidative stress and AR expression (Ihsan et al 2011).…”

Section: Ar Overexpressionmentioning

confidence: 98%

Pro-survival and anti-apoptotic properties of androgen receptor signaling by oxidative stress promote treatment resistance in prostate cancer

Shiota

Yokomizo

Naito

2012

Endocrine-Related Cancer

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Oxidative stress caused by an increase in reactive oxygen species levels or a decrease in cellular antioxidant capacity can evoke the modulation of various cellular events including androgen receptor (AR) signaling via direct or indirect interactions. In this review, we summarize the mechanisms of AR activation by oxidative stress including: i) AR overexpression; ii) AR activation by AR co-regulators or intracellular signal transduction pathways; iii) generation of AR mutations or splice variants; and iv) de novo androgen synthesis. AR signaling augmented by oxidative stress appears to contribute to pro-survival and anti-apoptotic effects in prostate cancer cells in response to androgen deprivation therapy. In addition, AR signaling suppresses anti-survival and pro-apoptotic effects in prostate cancer cells in response to various cytotoxic and tumorsuppressive interventions including taxanes and radiation through the modulation of bIII-tubulin and ataxia telangiectasia-mutated kinase expression respectively. Taken together, AR signaling appears to render prostate cancer cells refractory to various therapeutic interventions including castration, taxanes, and radiation, indicating that AR signaling is a comprehensive resistant factor and crucial target for prostate cancer treatment.

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Quantitative and immunohistochemical evaluation of PCNA, androgen receptors, apoptosis, and Glutathione-S-Transferase P1 on preneoplastic changes induced by cadmium and zinc chloride in the rat ventral prostate

Cited by 24 publications

References 43 publications

Glutathione S-transferase: differential expression of α, μ, and π isoenzymes in benign prostate, prostatic intraepithelial neoplasia, and prostatic adenocarcinoma

Glutathione S-transferase: differential expression of α, μ, and π isoenzymes in benign prostate, prostatic intraepithelial neoplasia, and prostatic adenocarcinoma

Cadmium Induced Cell Apoptosis, DNA Damage, Decreased DNA Repair Capacity, and Genomic Instability during Malignant Transformation of Human Bronchial Epithelial Cells

Pro-survival and anti-apoptotic properties of androgen receptor signaling by oxidative stress promote treatment resistance in prostate cancer

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