The role of oxidative stress in prostate cancer

Gupta-Elera, Gaytri; Garrett, Andrew; Robison, Richard A.; O’Neill, Kim L.

doi:10.1097/cej.0b013e32834a8002

Cited by 114 publications

(86 citation statements)

References 45 publications

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“…Oxidative stress has been widely implicated in the initiation and progression of cancer (Seoane et al 2011, Gupta-Elera et al 2012. A significant increase in DCF green fluorescence was observed in MCF-7 cells when cultured in a high-glucose condition (25 mM) compared with a normal-glucose (5 mM) condition.…”

Section: High Glucose and Insulin Generates Ros In Mcf-7 And Mda-mb-2mentioning

confidence: 87%

High glucose and insulin differentially modulates proliferation in MCF-7 and MDA-MB-231 cells

Gupta

Tikoo

2013

Journal of Molecular Endocrinology

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Various preclinical and clinical studies have linked diabetes and breast cancer, but little is known regarding the molecular mechanism involved. This study aimed to investigate the effect of high glucose and insulin in breast cancer cells (MCF-7: non-invasive, hormone dependent, and MDA-MB-231: invasive, hormone independent). In contrast to MCF-7 cells, high glucose augmented proliferation of MDA-MB-231 cells as observed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and bromodeoxyuridine assays. The high-glucose condition led to increased expression of cyclin D1, de-phosphorylation of p38, and increased phosphorylation of ERK in MDA-MB-231 cells but not in MCF-7 cells. Interestingly, we observed increased phosphorylation of GSK-3b, NF-kB, and ERa only in MCF-7 cells, highlighting their role as potential targets in prevention of progression of breast cancer under a high-glucose and insulin condition. Furthermore, insulin treatment under a high-glucose condition resulted in increased histone H3 phosphorylation and de-acetylation only in MDA-MB-231 cells. Taken together, we provide the first evidence that high glucose and insulin promotes proliferation of MDA-MB-231 cells by differential alteration of GSK-3b, NF-kB, and ERa expression and histone H3 modifications, which may directly or indirectly modulate the expression of genes involved in its proliferation.

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Section: High Glucose and Insulin Generates Ros In Mcf-7 And Mda-mb-2mentioning

confidence: 87%

High glucose and insulin differentially modulates proliferation in MCF-7 and MDA-MB-231 cells

Gupta

Tikoo

2013

Journal of Molecular Endocrinology

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“…Accumulating evidences suggest that oxidative stress (OS), resulting from the imbalance of reactive oxygen species (ROS) production and cellular antioxidant defensive systems, is a key aging-associated factor on prostate diseases [1,2]. Cumulative ROS effect may contribute to lipids, proteins, and DNA damage.…”

Section: Introductionmentioning

confidence: 99%

Comparative Effects of Roystonea Regia (D-004) and Saw Palmetto Lipid Extracts On Blood Oxidative Variables in Men with Benign Prostate Hyperplasia (BPH)

Guzman¹

2013

iosrphr

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“…Most are a consequence of the natural aging process-age is the most significant risk factor for PCa development. In addition to the genetic causes already mentioned, factors that contribute to the carcinogenesis of PCa include inflammation (Gueron et al, 2012;Kazma et al, 2012;Sfanos and de Marzo, 2012), oxidative stress and DNA damage (Miyake et al, 2004;Lockett et al, 2006;Battisti et al, 2011;Gupta-Elera et al, 2012), telomere shortening and telomerase activity (Kageyama et al, 1997;Donaldson et al, 1999;Fordyce et al, 2005;Treat et al, 2010;Xu et al, 2011), genomic alterations (Boyd et al, 2012;Nyquist and Dehm, 2013), and epigenetic modifications (Okino et al, 2007;Goering et al, 2012). Efforts have been made to achieve a deep understanding of these factors and consequently improve diagnosis and management of patients.…”

Section: Underlying Prostate Cancer Development and Metastasis Formationmentioning

confidence: 99%

Prostate cancer: the need for biomarkers and new therapeutic targets

Felgueiras

Silva

Fardilha

2014

J. Zhejiang Univ. Sci. B

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Prostate cancer (PCa) incidence and mortality have decreased in recent years. Nonetheless, it remains one of the most prevalent cancers in men, being a disquieting cause of men's death worldwide. Changes in many cell signaling pathways have a predominant role in the onset, development, and progression of the disease. These include prominent pathways involved in the growth, apoptosis, and angiogenesis of the normal prostate gland, such as androgen and estrogen signaling, and other growth factor signaling pathways. Understanding the foundations of PCa is leading to the discovery of key molecules that could be used to improve patient management. The ideal scenario would be to have a panel of molecules, preferably detectable in body fluids, that are specific and sensitive biomarkers for PCa. In the early stages, androgen deprivation is the gold standard therapy. However, as the cancer progresses, it eventually becomes independent of androgens, and hormonal therapy fails. For this reason, androgen-independent PCa is still a major therapeutic challenge. By disrupting specific protein interactions or manipulating the expression of some key molecules, it might be possible to regulate tumor growth and metastasis formation, avoiding the systemic side effects of current therapies. Clinical trials are already underway to assess the efficacy of molecules specially designed to target key proteins or protein interactions. In this review, we address that recent progress made towards understanding PCa development and the molecular pathways underlying this pathology. We also discuss relevant molecular markers for the management of PCa and new therapeutic challenges.

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The role of oxidative stress in prostate cancer

Cited by 114 publications

References 45 publications

High glucose and insulin differentially modulates proliferation in MCF-7 and MDA-MB-231 cells

High glucose and insulin differentially modulates proliferation in MCF-7 and MDA-MB-231 cells

Comparative Effects of Roystonea Regia (D-004) and Saw Palmetto Lipid Extracts On Blood Oxidative Variables in Men with Benign Prostate Hyperplasia (BPH)

Prostate cancer: the need for biomarkers and new therapeutic targets

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