{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T23:59:51Z","timestamp":1790812791430,"version":"4.1.0"},"reference-count":36,"publisher":"Bioscientifica","issue":"5","content-domain":{"domain":["erc.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2013,10]]},"abstract":"<jats:p>\n                    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.\n                    <jats:italic>IGFBP2<\/jats:italic>\n                    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\n                    <jats:italic>IGFBP2<\/jats:italic>\n                    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\n                    <jats:italic>IGFBP2<\/jats:italic>\n                    gene promoter. This finding could have important implications in relation to therapeutic strategies as epigenetic modulation could be reversible.\n                  <\/jats:p>","DOI":"10.1530\/erc-13-0077","type":"journal-article","created":{"date-parts":[[2013,8,26]],"date-time":"2013-08-26T19:47:22Z","timestamp":1377546442000},"page":"741-751","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":76,"title":["Hyperglycaemia-induced chemoresistance of prostate cancer cells due to IGFBP2"],"prefix":"10.1530","volume":"20","author":[{"given":"K M","family":"Biernacka","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C C","family":"Uzoh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L","family":"Zeng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R 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