Epigenetics in Prostate Cancer: Biologic and Clinical Relevance

Jerónimo, Carmen; Bastian, Patrick J.; Bjartell, Anders; Carbone, Giuseppina M.; Catto, James W.F.; Clark, Susan J.; Henrique, Rui; Nelson, William G.; Shariat, Shahrokh F.

doi:10.1016/j.eururo.2011.06.035

Cited by 196 publications

(177 citation statements)

References 155 publications

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“…There has been considerable recent interest in the epigenetic alterations contributing to PCa (Jeronimo et al 2011). Environmental exposures including altered metabolic conditions can induce epigenetic alterations and these may affect disease progression and response to therapy.…”

Section: Discussionmentioning

confidence: 99%

Hyperglycaemia-induced chemoresistance of prostate cancer cells due to IGFBP2

Biernacka¹,

Uzoh²,

Zeng³

et al. 2013

Endocrine-Related Cancer

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Clinically relevant prostate cancer (PCa) is more frequent in Westernised societies and increasingly men have co-morbidities associated with a Western lifestyle, primarily diabetes, characterised by hyperinsulinaemia and hyperglycaemia. IGFs and their binding proteins (IGFBPs) are important mediators of the effects of nutrition on growth and play a key role in the development of PCa. We used DU145, PC3 and LNCaP PCa cell lines to examine how hyperglycaemia altered their response to docetaxel. Trypan Blue dye-exclusion assay was used to determine the percentage of cell death. Protein abundance was determined using western immunoblotting. Levels of IGFBP2 were measured using an ELISA. IGFBP2 gene silencing was achieved using siRNA technology. DNA methylation was assessed using combined bisulphide restriction analysis. Acetylation status of histones H3 and H4 associated with IGFBP2 gene was assessed using chromatin immunoprecipitation assay. Hyperglycaemia reduced docetaxel-induced apoptosis by 40% for DU145 cells and by 88% for LNCaP cells. This reduced cell death was mediated by a glucose-induced up-regulation of IGFBP2, as silencing IGFBP2 negated the survival effect of high glucose. Glucose increased IGFBP2 via increasing the acetylation of histones associated with the IGFBP2 gene promoter. This finding could have important implications in relation to therapeutic strategies as epigenetic modulation could be reversible.

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Section: Discussionmentioning

confidence: 99%

Hyperglycaemia-induced chemoresistance of prostate cancer cells due to IGFBP2

Biernacka¹,

Uzoh²,

Zeng³

et al. 2013

Endocrine-Related Cancer

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“…Novel approaches include genetic analyses from peripheral blood, either germline analyses or characterization of DNA/RNA from circulating tumor cells (CTCs), or free circulating nucleic acids. The genetic landscape, key genetic alterations, epigenetic events, and microRNAs (miRNAs) in PCa have been reviewed [4][5][6][7].…”

Section: Introductionmentioning

confidence: 99%

“…Due to the breadth of the topic and recent high-quality reviews, we have specifically focused on genomic tests that are already available or approaching the point of clinical use [4][5][6][7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Genomic Predictors of Outcome in Prostate Cancer

et al. 2015

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“…1 Epigenetic regulation of genes has long been recognized as one of the many causes of cancer development and progression in human tumor system including PCa. 2 The epigenetic regulation of specific genes in human cancer cells include DNA methylation and histone modifications, leading to the changes in the expression of genes without altering the DNA sequences. DNA methylation has been well studied for understanding the epigenetic mechanisms of gene regulation.…”

Section: Introductionmentioning

confidence: 99%