How can food extracts consumed in the Mediterranean and East Asia suppress prostate cancer proliferation?
We have developed a blend of food extracts commonly consumed in the Mediterranean and East Asia, named blueberry punch (BBP), with the ultimate aim to formulate a chemoprevention strategy to inhibit prostate cancer progression in men on active surveillance protocol. We demonstrated previously that B...
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| Veröffentlicht in: | British journal of nutrition 2012-08, Vol.108 (3), p.424-430 |
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| creator | Yao, Mu Xie, Chanlu Constantine, Maryrose Hua, Sheng Hambly, Brett D. Jardine, Greg Sved, Paul Dong, Qihan |
| description | We have developed a blend of food extracts commonly consumed in the Mediterranean and East Asia, named blueberry punch (BBP), with the ultimate aim to formulate a chemoprevention strategy to inhibit prostate cancer progression in men on active surveillance protocol. We demonstrated previously that BBP inhibited prostate cancer cell proliferation in vitro and in vivo. The purpose of this study was to determine the molecular mechanism responsible for the suppression of prostate cancer cell proliferation by BBP. Treatment of lymph node-metastasised prostate cancer cells (LNCaP) and bone-metastasised prostate cancer cells (PC-3 and MDA-PCa-2b) with BBP (up to 0·8 %) for 72 h increased the percentage of cells at the G0/G1 phase and decreased those at the S and G2/M phases. The finding was supported by the reduction in the percentage of Ki-67-positive cells and of DNA synthesis measured by the incorporation of 5-ethynyl-2′-deoxyuridine. Concomitantly, BBP treatment decreased the protein levels of phosphorylated retinoblastoma, cyclin D1 and E, cyclin-dependent kinase (CDK) 4 and 2, and pre-replication complex (CDC6 and MCM7) in LNCaP and PC-3 cells, whereas CDK inhibitor p27 was elevated in these cell lines. In conclusion, BBP exerts its anti-proliferative effect on prostate cancer cells by modulating the expression and phosphorylation of multiple regulatory proteins essential for cell proliferation. |
| doi_str_mv | 10.1017/S0007114511005770 |
| format | Article |
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We demonstrated previously that BBP inhibited prostate cancer cell proliferation in vitro and in vivo. The purpose of this study was to determine the molecular mechanism responsible for the suppression of prostate cancer cell proliferation by BBP. Treatment of lymph node-metastasised prostate cancer cells (LNCaP) and bone-metastasised prostate cancer cells (PC-3 and MDA-PCa-2b) with BBP (up to 0·8 %) for 72 h increased the percentage of cells at the G0/G1 phase and decreased those at the S and G2/M phases. The finding was supported by the reduction in the percentage of Ki-67-positive cells and of DNA synthesis measured by the incorporation of 5-ethynyl-2′-deoxyuridine. Concomitantly, BBP treatment decreased the protein levels of phosphorylated retinoblastoma, cyclin D1 and E, cyclin-dependent kinase (CDK) 4 and 2, and pre-replication complex (CDC6 and MCM7) in LNCaP and PC-3 cells, whereas CDK inhibitor p27 was elevated in these cell lines. In conclusion, BBP exerts its anti-proliferative effect on prostate cancer cells by modulating the expression and phosphorylation of multiple regulatory proteins essential for cell proliferation.</description><identifier>ISSN: 0007-1145</identifier><identifier>EISSN: 1475-2662</identifier><identifier>DOI: 10.1017/S0007114511005770</identifier><identifier>PMID: 22067725</identifier><identifier>CODEN: BJNUAV</identifier><language>eng</language><publisher>Cambridge, UK: Cambridge University Press</publisher><subject>Antineoplastic Agents, Phytogenic - administration & dosage ; Antineoplastic Agents, Phytogenic - chemistry ; Antineoplastic Agents, Phytogenic - pharmacology ; Antioxidants ; Biological and medical sciences ; Cell Cycle - drug effects ; Cell Cycle Proteins - genetics ; Cell Cycle Proteins - metabolism ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Cellular biology ; Cyclin-Dependent Kinase Inhibitor Proteins - genetics ; Cyclin-Dependent Kinase Inhibitor Proteins - metabolism ; Cyclin-Dependent Kinases - genetics ; Cyclin-Dependent Kinases - metabolism ; Cyclins - genetics ; Cyclins - metabolism ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - metabolism ; Dose-Response Relationship, Drug ; Far East ; Feeding. Feeding behavior ; Food Analysis ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation - physiology ; Humans ; Male ; Mediterranean Region ; Minichromosome Maintenance Complex Component 7 ; Molecular Nutrition ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Plant Extracts - administration & dosage ; Plant Extracts - chemistry ; Plant Extracts - pharmacology ; Prostate cancer ; Prostatic Neoplasms - prevention & control ; Vaccinium ; Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><ispartof>British journal of nutrition, 2012-08, Vol.108 (3), p.424-430</ispartof><rights>Copyright © The Authors 2011</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c479t-199850b4437c3d23751db77024d566793a1a865899413cdd90d90f4cf47800a63</citedby><cites>FETCH-LOGICAL-c479t-199850b4437c3d23751db77024d566793a1a865899413cdd90d90f4cf47800a63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.cambridge.org/core/product/identifier/S0007114511005770/type/journal_article$$EHTML$$P50$$Gcambridge$$H</linktohtml><link.rule.ids>164,314,780,784,27923,27924,55627</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26212382$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22067725$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yao, Mu</creatorcontrib><creatorcontrib>Xie, Chanlu</creatorcontrib><creatorcontrib>Constantine, Maryrose</creatorcontrib><creatorcontrib>Hua, Sheng</creatorcontrib><creatorcontrib>Hambly, Brett D.</creatorcontrib><creatorcontrib>Jardine, Greg</creatorcontrib><creatorcontrib>Sved, Paul</creatorcontrib><creatorcontrib>Dong, Qihan</creatorcontrib><title>How can food extracts consumed in the Mediterranean and East Asia suppress prostate cancer proliferation?</title><title>British journal of nutrition</title><addtitle>Br J Nutr</addtitle><description>We have developed a blend of food extracts commonly consumed in the Mediterranean and East Asia, named blueberry punch (BBP), with the ultimate aim to formulate a chemoprevention strategy to inhibit prostate cancer progression in men on active surveillance protocol. We demonstrated previously that BBP inhibited prostate cancer cell proliferation in vitro and in vivo. The purpose of this study was to determine the molecular mechanism responsible for the suppression of prostate cancer cell proliferation by BBP. Treatment of lymph node-metastasised prostate cancer cells (LNCaP) and bone-metastasised prostate cancer cells (PC-3 and MDA-PCa-2b) with BBP (up to 0·8 %) for 72 h increased the percentage of cells at the G0/G1 phase and decreased those at the S and G2/M phases. The finding was supported by the reduction in the percentage of Ki-67-positive cells and of DNA synthesis measured by the incorporation of 5-ethynyl-2′-deoxyuridine. Concomitantly, BBP treatment decreased the protein levels of phosphorylated retinoblastoma, cyclin D1 and E, cyclin-dependent kinase (CDK) 4 and 2, and pre-replication complex (CDC6 and MCM7) in LNCaP and PC-3 cells, whereas CDK inhibitor p27 was elevated in these cell lines. In conclusion, BBP exerts its anti-proliferative effect on prostate cancer cells by modulating the expression and phosphorylation of multiple regulatory proteins essential for cell proliferation.</description><subject>Antineoplastic Agents, Phytogenic - administration & dosage</subject><subject>Antineoplastic Agents, Phytogenic - chemistry</subject><subject>Antineoplastic Agents, Phytogenic - pharmacology</subject><subject>Antioxidants</subject><subject>Biological and medical sciences</subject><subject>Cell Cycle - drug effects</subject><subject>Cell Cycle Proteins - genetics</subject><subject>Cell Cycle Proteins - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Cellular biology</subject><subject>Cyclin-Dependent Kinase Inhibitor Proteins - genetics</subject><subject>Cyclin-Dependent Kinase Inhibitor Proteins - metabolism</subject><subject>Cyclin-Dependent Kinases - genetics</subject><subject>Cyclin-Dependent Kinases - metabolism</subject><subject>Cyclins - genetics</subject><subject>Cyclins - metabolism</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Dose-Response Relationship, Drug</subject><subject>Far East</subject><subject>Feeding. 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Feeding behavior</topic><topic>Food Analysis</topic><topic>Fundamental and applied biological sciences. 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We demonstrated previously that BBP inhibited prostate cancer cell proliferation in vitro and in vivo. The purpose of this study was to determine the molecular mechanism responsible for the suppression of prostate cancer cell proliferation by BBP. Treatment of lymph node-metastasised prostate cancer cells (LNCaP) and bone-metastasised prostate cancer cells (PC-3 and MDA-PCa-2b) with BBP (up to 0·8 %) for 72 h increased the percentage of cells at the G0/G1 phase and decreased those at the S and G2/M phases. The finding was supported by the reduction in the percentage of Ki-67-positive cells and of DNA synthesis measured by the incorporation of 5-ethynyl-2′-deoxyuridine. Concomitantly, BBP treatment decreased the protein levels of phosphorylated retinoblastoma, cyclin D1 and E, cyclin-dependent kinase (CDK) 4 and 2, and pre-replication complex (CDC6 and MCM7) in LNCaP and PC-3 cells, whereas CDK inhibitor p27 was elevated in these cell lines. In conclusion, BBP exerts its anti-proliferative effect on prostate cancer cells by modulating the expression and phosphorylation of multiple regulatory proteins essential for cell proliferation.</abstract><cop>Cambridge, UK</cop><pub>Cambridge University Press</pub><pmid>22067725</pmid><doi>10.1017/S0007114511005770</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Antineoplastic Agents, Phytogenic - administration & dosage Antineoplastic Agents, Phytogenic - chemistry Antineoplastic Agents, Phytogenic - pharmacology Antioxidants Biological and medical sciences Cell Cycle - drug effects Cell Cycle Proteins - genetics Cell Cycle Proteins - metabolism Cell Line, Tumor Cell Proliferation - drug effects Cellular biology Cyclin-Dependent Kinase Inhibitor Proteins - genetics Cyclin-Dependent Kinase Inhibitor Proteins - metabolism Cyclin-Dependent Kinases - genetics Cyclin-Dependent Kinases - metabolism Cyclins - genetics Cyclins - metabolism DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Dose-Response Relationship, Drug Far East Feeding. Feeding behavior Food Analysis Fundamental and applied biological sciences. Psychology Gene Expression Regulation - physiology Humans Male Mediterranean Region Minichromosome Maintenance Complex Component 7 Molecular Nutrition Nuclear Proteins - genetics Nuclear Proteins - metabolism Plant Extracts - administration & dosage Plant Extracts - chemistry Plant Extracts - pharmacology Prostate cancer Prostatic Neoplasms - prevention & control Vaccinium Vertebrates: anatomy and physiology, studies on body, several organs or systems |
| title | How can food extracts consumed in the Mediterranean and East Asia suppress prostate cancer proliferation? |
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