Antioxidant enzyme expression and reactive oxygen species damage in prostatic intraepithelial neoplasia and cancer

Bostwick, David G.; Alexander, Erik E.; Singh, Rajesh Kumar; Shan, Ailin; Qian, Junqi; Santella, Regina M.; Oberley, Larry W.; Yan, Tao; Zhong, Weixiong; Jiang, Bo; Oberley, Terry D.

doi:10.1002/1097-0142(20000701)89:1<123::aid-cncr17>3.0.co;2-9

Cited by 231 publications

(111 citation statements)

References 44 publications

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“…induction of proliferation and of genomic instability. As the compartment with relatively high local concentration of catalase in close vicinity of the cell membrane represents a very minor part of the total mass of the tumor cell, the finding of high concentration of catalase on the outside of the membrane is still consistent with the established finding that the average concentration of catalase in tumor cells is usually lower than in normal cells (Sato et al, 1992;Coursin et al, 1996;Baker et al, 1997;Bostwick et al, 2000;Chung-Man et al, 2001;Cullen et al, 2003;Kwei et al, 2004). Therefore, the findings by Deichman's group (Deichman and Vendrov, 1986;Deichman et al, 1989Deichman et al, , 1998Deichman, 2000Deichman, , 2002 and our own findings (Bechtel and Bauer, 2009;Heinzelmann and Bauer, 2010) are not discrepant to the findings by Sato et al (1992), Coursin et al (1996), Baker et al (1997), Bostwick et al (2000), Chung-Man et al (2001), Cullen et al (2003), and Kwei et al (2004), but rather are focused on a specific site on tumor cells with biologically relevant high catalase expression that is dramatically different from the much lower catalase expression inside the cell.…”

Section: Discussionsupporting

confidence: 71%

“…normal nontransformed cells, transformed cells, and bona vide tumor cells to experimentally address the question whether translocation of catalase to the outside of the cell membrane is acquired at the early step of oncogenic transformation of the cells to the malignant state or later, during successful tumor formation and progression. In addition, this study aimed to clarify the nature of the discrepancy between the finding that tumor progression caused increased resistance against H 2 O 2 and peroxynitrite (Deichman and Vendrov, 1986;Deichman et al, 1989Deichman et al, , 1998Deichman, 2000Deichman, , 2002Heinzelmann and Bauer, 2010;Bauer, 2012) and the frequently published finding of overall lower total concentration of catalase in tumor cells compared to normal tissue (Sato et al, 1992;Coursin et al, 1996;Baker et al, 1997;Bostwick et al, 2000;Chung-Man et al, 2001;Ho et al, 2001;Cullen et al, 2003;Kwei et al, 2004).…”

Section: Introductionmentioning

confidence: 95%

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Extracellular localization of catalase is associated with the transformed state of malignant cells

Böhm¹,

Heinzelmann²,

Motz³

et al. 2015

Biological Chemistry

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Oncogenic transformation is dependent on activated membrane-associated NADPH oxidase (NOX). However, the resultant extracellular superoxide anions are also driving the NO/peroxynitrite and the HOCl pathway, which eliminates NOX-expressing transformed cells through selective apoptosis induction. Tumor progression is dependent on dominant interference with intercellular apoptosis-inducing ROS signaling through membraneassociated catalase, which decomposes H 2 O 2 and peroxynitrite and oxidizes NO. Particularly, the decomposition of extracellular peroxynitrite strictly requires membraneassociated catalase. We utilized small interfering RNA (siRNA)-mediated knockdown of catalase and neutralizing antibodies directed against the enzyme in combination with challenging H 2 O 2 or peroxynitrite to determine activity and localization of catalase in cells from three distinct steps of multistage oncogenesis. Nontransformed cells did not generate extracellular superoxide anions and only showed intracellular catalase activity. Transformed cells showed superoxide anion-dependent intercellular apoptosis-inducing ROS signaling in the presence of suboptimal catalase activity in their membrane. Tumor cells exhibited tight control of intercellular apoptosis-inducing ROS signaling through a high local concentration of membrane-associated catalase. These data demonstrate that translocation of catalase to the outside of the cell membrane is already associated with the transformation step. A strong local increase in the concentration of membrane-associated catalase is achieved during tumor progression and is controlled by tumor cell-derived H 2 O 2 and by transglutaminase.

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Section: Discussionsupporting

confidence: 71%

Section: Introductionmentioning

confidence: 95%

Extracellular localization of catalase is associated with the transformed state of malignant cells

Böhm¹,

Heinzelmann²,

Motz³

et al. 2015

Biological Chemistry

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“…Oxidative stress has been shown to play an important role in the tumorigenesis and progression of prostate cancer (Bostwick et al 2000, Sharifi et al 2008, Khandrika et al 2009), as well as in the conversion of androgen-dependent prostate cancer into CRPC (Sharifi et al 2008, Shiota et al 2010, 2011a. Together, these results suggest an intimate cross-talk between oxidative stress and AR signaling.…”

Section: Introductionmentioning

confidence: 85%

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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“…Reactive oxygen species produced during chronic inflammation and other mechanisms involving oxidative stress may play an important role in prostate carcinogenesis. SODs are expressed in many human organs, including the prostate (1,2). Thus, SOD genes are good candidates to evaluate genetic susceptibility for prostate cancer.…”

Section: Introductionmentioning

confidence: 99%

Functional Variant of Manganese Superoxide Dismutase (SOD2 V16A) Polymorphism Is Associated with Prostate Cancer Risk in the Prostate, Lung, Colorectal, and Ovarian Cancer Study

Kang

Lee

Park

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

125

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Superoxide dismutase (SOD) plays a key role in the detoxification of superoxide free radicals. We evaluated the association of prostate cancer with genetic polymorphisms in SOD1 (CuZn-SOD; IVS3-251A>G), SOD2 [MnSOD; Ex2+24T>C (V16A)], and SOD3 (EC-SOD; IVS1+186C>T, Ex3-631C>G, Ex3-516C>T, and Ex3-489C>T), the three main isoforms of SOD. Prostate cancer cases (n = 1,320) from the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial were frequency matched to nondiseased controls (n = 1,842) by age, race, time since initial screening, and year of blood draw. Conditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (95% CI); stratified analysis by the level of antioxidative vitamins was also conducted. The higher activity Ala variant at SOD2 Ex2+24T>C (V16A), which has been hypothesized to suppress prostate carcinogenesis, was associated with elevation of prostate cancer risk in Caucasians (Val/Ala versus Val/Val: OR, 1.17; 95% CI, 0.97-1.42; Ala/Ala versus Val/Val: OR, 1.28; 95% CI, 1.03-1.60; P trend = 0.03). Stratification by quartiles of dietary and supplemental vitamin E intake (IU/d) showed risks of prostate cancer tended to be increased among SOD2 Ala allele carriers, except at the highest quartile of vitamin E intake (>222; P interaction = 0.06, Q1-Q3 versus Q4). The association between Ala allele and prostate cancer risk among those with lower intake of vitamin E (V222) was stronger for smokers (OR, 1.44; 95% CI, 1.10-1.90). No significant association with prostate cancer was observed for polymorphic variants in SOD3 or SOD1. These results suggest that the Ala variant of SOD2 is associated with moderately increased risk of prostate cancer, particularly among men with lower intakes of dietary and supplemental vitamin E. (Cancer Epidemiol Biomarkers Prev 2007;16(8):1581-6)

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Antioxidant enzyme expression and reactive oxygen species damage in prostatic intraepithelial neoplasia and cancer

Cited by 231 publications

References 44 publications

Extracellular localization of catalase is associated with the transformed state of malignant cells

Extracellular localization of catalase is associated with the transformed state of malignant cells

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

Functional Variant of Manganese Superoxide Dismutase (SOD2 V16A) Polymorphism Is Associated with Prostate Cancer Risk in the Prostate, Lung, Colorectal, and Ovarian Cancer Study

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