Compound K, a metabolite of ginseng saponin, inhibits colorectal cancer cell growth and induces apoptosis through inhibition of histone deacetylase activity
In this study, we investigated the molecular mechanisms underlying the anti-proliferative effects of Compound K, with specific reference to histone modification. Exposure of HT-29 human colon cancer cells to Compound K resulted in time-dependent inhibition of histone deacetylase (HDAC) activity, mRN...
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| Veröffentlicht in: | International journal of oncology 2013-12, Vol.43 (6), p.1907-1914 |
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| container_title | International journal of oncology |
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| creator | KANG, KYOUNG AH PIAO, MEI JING KIM, KI CHEON ZHENG, JIAN YAO, CHENG WEN CHA, JI WON KIM, HYE SUN KIM, DONG HYUN BAE, SUK CHUL HYUN, JIN WON |
| description | In this study, we investigated the molecular mechanisms underlying the anti-proliferative effects of Compound K, with specific reference to histone modification. Exposure of HT-29 human colon cancer cells to Compound K resulted in time-dependent inhibition of histone deacetylase (HDAC) activity, mRNA and protein expression. Compound K treatment induced unmethylation of the RUNX3 promoter region such as TSA treatment and an accumulation of acetylated histones H3 and H4 within the total cellular chromatin, resulting in an enhanced ability of these histones to bind to the promoter sequences of the tumor suppressor gene Runt-related transcription factor 3 (RUNX3). Treatment of cells with Compound K increased the mRNA and protein expression of RUNX3, as well as p21, a downstream target of RUNX3. These alterations were consistent with cell cycle arrest at the G0/G1 phases and induction of apoptosis. Our results provide new insights into the mechanisms of Compound K action in human colorectal cancer cells and suggest that HDAC inhibition presents a novel approach to prevent or treat colorectal cancer. |
| doi_str_mv | 10.3892/ijo.2013.2129 |
| format | Article |
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Exposure of HT-29 human colon cancer cells to Compound K resulted in time-dependent inhibition of histone deacetylase (HDAC) activity, mRNA and protein expression. Compound K treatment induced unmethylation of the RUNX3 promoter region such as TSA treatment and an accumulation of acetylated histones H3 and H4 within the total cellular chromatin, resulting in an enhanced ability of these histones to bind to the promoter sequences of the tumor suppressor gene Runt-related transcription factor 3 (RUNX3). Treatment of cells with Compound K increased the mRNA and protein expression of RUNX3, as well as p21, a downstream target of RUNX3. These alterations were consistent with cell cycle arrest at the G0/G1 phases and induction of apoptosis. Our results provide new insights into the mechanisms of Compound K action in human colorectal cancer cells and suggest that HDAC inhibition presents a novel approach to prevent or treat colorectal cancer.</description><identifier>ISSN: 1019-6439</identifier><identifier>EISSN: 1791-2423</identifier><identifier>DOI: 10.3892/ijo.2013.2129</identifier><identifier>PMID: 24100442</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Acetylation - drug effects ; Apoptosis ; Apoptosis - drug effects ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Chromatin ; Colorectal cancer ; Colorectal Neoplasms - drug therapy ; Compound K ; Core Binding Factor Alpha 3 Subunit - genetics ; Core Binding Factor Alpha 3 Subunit - metabolism ; Cyclin-Dependent Kinase Inhibitor p21 - genetics ; Deoxyribonucleic acid ; DNA ; DNA methylation ; DNA-Binding Proteins - metabolism ; Epigenetics ; G1 Phase Cell Cycle Checkpoints - drug effects ; Gene expression ; Gene Expression Regulation, Neoplastic - drug effects ; Ginsenosides - pharmacology ; histone deacetylase ; Histone Deacetylase Inhibitors - pharmacology ; Histone Deacetylases - drug effects ; Histone Deacetylases - metabolism ; Histones - metabolism ; HT29 Cells ; Humans ; Hydroxamic Acids - pharmacology ; Kinases ; Medical prognosis ; Panax ; Promoter Regions, Genetic - drug effects ; Promoter Regions, Genetic - genetics ; Protein Binding - drug effects ; Proteins ; RNA, Messenger - biosynthesis ; Runt-related transcription factor ; Studies ; Transcription factors</subject><ispartof>International journal of oncology, 2013-12, Vol.43 (6), p.1907-1914</ispartof><rights>Copyright © 2013, Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c458t-7efbe769db7f3fed22156a79d750e212da07b24156b2a63d4d6c1508b0b628f03</citedby><cites>FETCH-LOGICAL-c458t-7efbe769db7f3fed22156a79d750e212da07b24156b2a63d4d6c1508b0b628f03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,5555,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24100442$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KANG, KYOUNG AH</creatorcontrib><creatorcontrib>PIAO, MEI JING</creatorcontrib><creatorcontrib>KIM, KI CHEON</creatorcontrib><creatorcontrib>ZHENG, JIAN</creatorcontrib><creatorcontrib>YAO, CHENG WEN</creatorcontrib><creatorcontrib>CHA, JI WON</creatorcontrib><creatorcontrib>KIM, HYE SUN</creatorcontrib><creatorcontrib>KIM, DONG HYUN</creatorcontrib><creatorcontrib>BAE, SUK CHUL</creatorcontrib><creatorcontrib>HYUN, JIN WON</creatorcontrib><title>Compound K, a metabolite of ginseng saponin, inhibits colorectal cancer cell growth and induces apoptosis through inhibition of histone deacetylase activity</title><title>International journal of oncology</title><addtitle>Int J Oncol</addtitle><description>In this study, we investigated the molecular mechanisms underlying the anti-proliferative effects of Compound K, with specific reference to histone modification. Exposure of HT-29 human colon cancer cells to Compound K resulted in time-dependent inhibition of histone deacetylase (HDAC) activity, mRNA and protein expression. Compound K treatment induced unmethylation of the RUNX3 promoter region such as TSA treatment and an accumulation of acetylated histones H3 and H4 within the total cellular chromatin, resulting in an enhanced ability of these histones to bind to the promoter sequences of the tumor suppressor gene Runt-related transcription factor 3 (RUNX3). Treatment of cells with Compound K increased the mRNA and protein expression of RUNX3, as well as p21, a downstream target of RUNX3. These alterations were consistent with cell cycle arrest at the G0/G1 phases and induction of apoptosis. Our results provide new insights into the mechanisms of Compound K action in human colorectal cancer cells and suggest that HDAC inhibition presents a novel approach to prevent or treat colorectal cancer.</description><subject>Acetylation - drug effects</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Chromatin</subject><subject>Colorectal cancer</subject><subject>Colorectal Neoplasms - drug therapy</subject><subject>Compound K</subject><subject>Core Binding Factor Alpha 3 Subunit - genetics</subject><subject>Core Binding Factor Alpha 3 Subunit - metabolism</subject><subject>Cyclin-Dependent Kinase Inhibitor p21 - genetics</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA methylation</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Epigenetics</subject><subject>G1 Phase Cell Cycle Checkpoints - drug effects</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Ginsenosides - pharmacology</subject><subject>histone deacetylase</subject><subject>Histone Deacetylase Inhibitors - pharmacology</subject><subject>Histone Deacetylases - drug effects</subject><subject>Histone Deacetylases - metabolism</subject><subject>Histones - metabolism</subject><subject>HT29 Cells</subject><subject>Humans</subject><subject>Hydroxamic Acids - pharmacology</subject><subject>Kinases</subject><subject>Medical prognosis</subject><subject>Panax</subject><subject>Promoter Regions, Genetic - drug effects</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Protein Binding - drug effects</subject><subject>Proteins</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Runt-related transcription factor</subject><subject>Studies</subject><subject>Transcription factors</subject><issn>1019-6439</issn><issn>1791-2423</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNo9kTtvFDEURi0EIiFQ0iJLFDTx4td41iVa8RKRaKAe-XFnx6tZe7A9RPtf-LF4tUmq6-L4XN3vQ-gtoxux1fxjOKQNp0xsOOP6GbpmvWaESy6etzdlmigp9BV6VcqBUt51lL1EV1wySqXk1-jfLh2XtEaPf9xig49QjU1zqIDTiPchFoh7XMySYoi3OMQp2FALdmlOGVw1M3YmOsjYwTzjfU73dcKm6UL0q4OC29elphIKrlNO6356lIQUzzumUGqKgD0YB_U0mwLYuBr-hnp6jV6MZi7w5mHeoN9fPv_afSN3P79-3326I05220p6GC30Snvbj2IEzznrlOm17zsKLRZvaG_byZ2y3CjhpVeOdXRrqVV8O1Jxg95fvEtOf1YodTikNce2cmBacCGkVKpR5EK5nErJMA5LDkeTTwOjw7mLoXUxnLsYzl00_t2DdbVH8E_0Y_gN-HABytISCz6VJ6aZiBSEKsI07cV_fLqVCQ</recordid><startdate>20131201</startdate><enddate>20131201</enddate><creator>KANG, KYOUNG AH</creator><creator>PIAO, MEI JING</creator><creator>KIM, KI CHEON</creator><creator>ZHENG, JIAN</creator><creator>YAO, CHENG WEN</creator><creator>CHA, JI WON</creator><creator>KIM, HYE SUN</creator><creator>KIM, DONG HYUN</creator><creator>BAE, SUK CHUL</creator><creator>HYUN, JIN WON</creator><general>D.A. 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drug effects</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Chromatin</topic><topic>Colorectal cancer</topic><topic>Colorectal Neoplasms - drug therapy</topic><topic>Compound K</topic><topic>Core Binding Factor Alpha 3 Subunit - genetics</topic><topic>Core Binding Factor Alpha 3 Subunit - metabolism</topic><topic>Cyclin-Dependent Kinase Inhibitor p21 - genetics</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA methylation</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Epigenetics</topic><topic>G1 Phase Cell Cycle Checkpoints - drug effects</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Ginsenosides - pharmacology</topic><topic>histone deacetylase</topic><topic>Histone Deacetylase Inhibitors - pharmacology</topic><topic>Histone Deacetylases - 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Exposure of HT-29 human colon cancer cells to Compound K resulted in time-dependent inhibition of histone deacetylase (HDAC) activity, mRNA and protein expression. Compound K treatment induced unmethylation of the RUNX3 promoter region such as TSA treatment and an accumulation of acetylated histones H3 and H4 within the total cellular chromatin, resulting in an enhanced ability of these histones to bind to the promoter sequences of the tumor suppressor gene Runt-related transcription factor 3 (RUNX3). Treatment of cells with Compound K increased the mRNA and protein expression of RUNX3, as well as p21, a downstream target of RUNX3. These alterations were consistent with cell cycle arrest at the G0/G1 phases and induction of apoptosis. Our results provide new insights into the mechanisms of Compound K action in human colorectal cancer cells and suggest that HDAC inhibition presents a novel approach to prevent or treat colorectal cancer.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>24100442</pmid><doi>10.3892/ijo.2013.2129</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Acetylation - drug effects Apoptosis Apoptosis - drug effects Cell cycle Cell growth Cell Line, Tumor Cell Proliferation - drug effects Chromatin Colorectal cancer Colorectal Neoplasms - drug therapy Compound K Core Binding Factor Alpha 3 Subunit - genetics Core Binding Factor Alpha 3 Subunit - metabolism Cyclin-Dependent Kinase Inhibitor p21 - genetics Deoxyribonucleic acid DNA DNA methylation DNA-Binding Proteins - metabolism Epigenetics G1 Phase Cell Cycle Checkpoints - drug effects Gene expression Gene Expression Regulation, Neoplastic - drug effects Ginsenosides - pharmacology histone deacetylase Histone Deacetylase Inhibitors - pharmacology Histone Deacetylases - drug effects Histone Deacetylases - metabolism Histones - metabolism HT29 Cells Humans Hydroxamic Acids - pharmacology Kinases Medical prognosis Panax Promoter Regions, Genetic - drug effects Promoter Regions, Genetic - genetics Protein Binding - drug effects Proteins RNA, Messenger - biosynthesis Runt-related transcription factor Studies Transcription factors |
| title | Compound K, a metabolite of ginseng saponin, inhibits colorectal cancer cell growth and induces apoptosis through inhibition of histone deacetylase activity |
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