Resveratrol inhibits the growth of gastric cancer by inducing G1 phase arrest and senescence in a Sirt1-dependent manner
Resveratrol, a naturally occurring polyphenolic compound, has been reported to exert anticancer activity by affecting diverse molecular targets. In this study, we examined the effects and the underlying mechanisms of resveratrol on gastric cancer. We found that resveratrol inhibited the proliferatio...
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| description | Resveratrol, a naturally occurring polyphenolic compound, has been reported to exert anticancer activity by affecting diverse molecular targets. In this study, we examined the effects and the underlying mechanisms of resveratrol on gastric cancer. We found that resveratrol inhibited the proliferation of gastric cancer cells in a dose-dependent manner. At the concentration of 25 and 50 µM, resveratrol inhibited the cell viability and diminished the clonogenic potential of gastric cancer cells. Resveratrol treatment arrested gastric cancer cells in the G1 phase and led to senescence instead of apoptosis. Regulators of the cell cycle and senescence pathways, including cyclin D1, cyclin-dependent kinase (CDK4 and 6), p21 and p16, were dysregulated by resveratrol treatment. The inhibitory effects of resveratrol on gastric cancer were also verified in vivo using a nude mice xenograft model. Resveratrol (40 mg/kg/d) exerted inhibitory activities on gastric cancer development and significantly decreased the fractions of Ki67-positive cells in the tumor specimens from the nude mice. After resveratrol treatment, the induction of senescence and the changes in the expression of the regulators involved in the cell cycle and senescence pathways were similar to what we observed in vitro. However, the depletion of Sirtuin (Sirt)1 reversed the above-described effects of resveratrol both in vitro and in vivo. Our data suggest that resveratrol inhibits gastric cancer in a Sirt1-dependent manner and provide detailed evidence for the possibility of applying resveratrol in gastric cancer prevention and therapy. |
| doi_str_mv | 10.1371/journal.pone.0070627 |
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In this study, we examined the effects and the underlying mechanisms of resveratrol on gastric cancer. We found that resveratrol inhibited the proliferation of gastric cancer cells in a dose-dependent manner. At the concentration of 25 and 50 µM, resveratrol inhibited the cell viability and diminished the clonogenic potential of gastric cancer cells. Resveratrol treatment arrested gastric cancer cells in the G1 phase and led to senescence instead of apoptosis. Regulators of the cell cycle and senescence pathways, including cyclin D1, cyclin-dependent kinase (CDK4 and 6), p21 and p16, were dysregulated by resveratrol treatment. The inhibitory effects of resveratrol on gastric cancer were also verified in vivo using a nude mice xenograft model. Resveratrol (40 mg/kg/d) exerted inhibitory activities on gastric cancer development and significantly decreased the fractions of Ki67-positive cells in the tumor specimens from the nude mice. After resveratrol treatment, the induction of senescence and the changes in the expression of the regulators involved in the cell cycle and senescence pathways were similar to what we observed in vitro. However, the depletion of Sirtuin (Sirt)1 reversed the above-described effects of resveratrol both in vitro and in vivo. Our data suggest that resveratrol inhibits gastric cancer in a Sirt1-dependent manner and provide detailed evidence for the possibility of applying resveratrol in gastric cancer prevention and therapy.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0070627</identifier><identifier>PMID: 24278101</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Anticancer properties ; Antitumor activity ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - genetics ; Biochemistry ; Biology ; Blotting, Western ; Breast cancer ; Cancer ; Cancer prevention ; Cancer therapies ; Cancer treatment ; Cell cycle ; Cell Cycle - drug effects ; Cell Cycle - genetics ; Cell growth ; Cell Line, Tumor ; Cell proliferation ; Cell Survival - drug effects ; Cell Survival - genetics ; Cellular Senescence - drug effects ; Cellular Senescence - genetics ; Cyclin D1 ; Cyclin-dependent kinase 4 ; Diabetes ; Ethics ; Female ; G1 phase ; G1 Phase - drug effects ; G1 Phase - genetics ; Gastric cancer ; Health aspects ; Humans ; Immunohistochemistry ; Medicine ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Pathogens ; Pathways ; Regulators ; Resveratrol ; RNA, Small Interfering - genetics ; Senescence ; SIRT1 protein ; Sirtuin 1 - genetics ; Sirtuin 1 - metabolism ; Stilbenes - pharmacology ; Stilbenes - therapeutic use ; Stomach cancer ; Stomach Neoplasms - drug therapy ; Stomach Neoplasms - genetics ; Stomach Neoplasms - metabolism ; Xenograft Model Antitumor Assays ; Xenografts</subject><ispartof>PloS one, 2013-11, Vol.8 (11), p.e70627-e70627</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Yang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Yang et al 2013 Yang et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-32374315082279b76047c66291839232b7c273bf0d6977c9c4e85b665d244f013</citedby><cites>FETCH-LOGICAL-c758t-32374315082279b76047c66291839232b7c273bf0d6977c9c4e85b665d244f013</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3836800/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3836800/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2095,2914,23846,27903,27904,53770,53772,79347,79348</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24278101$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Heymann, Dominique</contributor><creatorcontrib>Yang, Qing</creatorcontrib><creatorcontrib>Wang, Bo</creatorcontrib><creatorcontrib>Zang, Wen</creatorcontrib><creatorcontrib>Wang, Xuping</creatorcontrib><creatorcontrib>Liu, Zhifang</creatorcontrib><creatorcontrib>Li, Wenjuan</creatorcontrib><creatorcontrib>Jia, Jihui</creatorcontrib><title>Resveratrol inhibits the growth of gastric cancer by inducing G1 phase arrest and senescence in a Sirt1-dependent manner</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Resveratrol, a naturally occurring polyphenolic compound, has been reported to exert anticancer activity by affecting diverse molecular targets. In this study, we examined the effects and the underlying mechanisms of resveratrol on gastric cancer. We found that resveratrol inhibited the proliferation of gastric cancer cells in a dose-dependent manner. At the concentration of 25 and 50 µM, resveratrol inhibited the cell viability and diminished the clonogenic potential of gastric cancer cells. Resveratrol treatment arrested gastric cancer cells in the G1 phase and led to senescence instead of apoptosis. Regulators of the cell cycle and senescence pathways, including cyclin D1, cyclin-dependent kinase (CDK4 and 6), p21 and p16, were dysregulated by resveratrol treatment. The inhibitory effects of resveratrol on gastric cancer were also verified in vivo using a nude mice xenograft model. Resveratrol (40 mg/kg/d) exerted inhibitory activities on gastric cancer development and significantly decreased the fractions of Ki67-positive cells in the tumor specimens from the nude mice. After resveratrol treatment, the induction of senescence and the changes in the expression of the regulators involved in the cell cycle and senescence pathways were similar to what we observed in vitro. However, the depletion of Sirtuin (Sirt)1 reversed the above-described effects of resveratrol both in vitro and in vivo. Our data suggest that resveratrol inhibits gastric cancer in a Sirt1-dependent manner and provide detailed evidence for the possibility of applying resveratrol in gastric cancer prevention and therapy.</description><subject>Animals</subject><subject>Anticancer properties</subject><subject>Antitumor activity</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>Biochemistry</subject><subject>Biology</subject><subject>Blotting, Western</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Cancer prevention</subject><subject>Cancer therapies</subject><subject>Cancer treatment</subject><subject>Cell cycle</subject><subject>Cell Cycle - drug effects</subject><subject>Cell Cycle - genetics</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Cell Survival - drug effects</subject><subject>Cell Survival - genetics</subject><subject>Cellular Senescence - 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drug therapy</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - metabolism</subject><subject>Xenograft Model Antitumor Assays</subject><subject>Xenografts</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk19v0zAUxSMEYqPwDRBYQkLw0OI_iZ28IE0TjEqTJm3Aq-U4N4mr1O5sZ2zfHnfNphbtAeUhkf0759on92bZW4IXhAnyZeVGb9Ww2DgLC4wF5lQ8y45JxeicU8ye730fZa9CWGFcsJLzl9kRzakoCSbH2e0lhBvwKno3IGN7U5sYUOwBdd79iT1yLepUiN5opJXV4FF9l8Bm1MZ26IygTa8CIOU9hIiUbVAAC0FDYhOHFLoyPpJ5AxuwDdiI1spa8K-zF60aAryZ3rPs1_dvP09_zM8vzpanJ-dzLYoyzhllImekwCWloqoFx7nQnNOKlKyijNZCU8HqFje8EkJXOoeyqDkvGprnLSZslr3f-W4GF-QUWpAk57jABUniWbbcEY1TK7nxZq38nXTKyPsF5zupfDR6AAm4KPK2VqkEyRUHVWNCGCFcVBVhUCWvr1O1sV5Dk1KIXg0Hpoc71vSyczeSlYyXGCeDT5OBd9djilSuTQpzGJQFN96fm5Ky4GyLfvgHffp2E9WpdAFjW5fq6q2pPMlTE4jUHjRRiyeo9DSwNjp1WGvS-oHg84EgMRFuY6fGEOTy6vL_2Yvfh-zHPbYHNcQ-uGGMxtlwCOY7UHsXgof2MWSC5XZAHtKQ2wGR04Ak2bv9H_QoepgI9hciXwiT</recordid><startdate>20131121</startdate><enddate>20131121</enddate><creator>Yang, Qing</creator><creator>Wang, Bo</creator><creator>Zang, Wen</creator><creator>Wang, Xuping</creator><creator>Liu, Zhifang</creator><creator>Li, Wenjuan</creator><creator>Jia, Jihui</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20131121</creationdate><title>Resveratrol inhibits the growth of gastric cancer by inducing G1 phase arrest and senescence in a Sirt1-dependent manner</title><author>Yang, Qing ; Wang, Bo ; Zang, Wen ; Wang, Xuping ; Liu, Zhifang ; Li, Wenjuan ; Jia, Jihui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-32374315082279b76047c66291839232b7c273bf0d6977c9c4e85b665d244f013</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Anticancer properties</topic><topic>Antitumor activity</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - genetics</topic><topic>Biochemistry</topic><topic>Biology</topic><topic>Blotting, Western</topic><topic>Breast cancer</topic><topic>Cancer</topic><topic>Cancer prevention</topic><topic>Cancer therapies</topic><topic>Cancer treatment</topic><topic>Cell cycle</topic><topic>Cell Cycle - drug effects</topic><topic>Cell Cycle - genetics</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Cell Survival - drug effects</topic><topic>Cell Survival - genetics</topic><topic>Cellular Senescence - drug effects</topic><topic>Cellular Senescence - genetics</topic><topic>Cyclin D1</topic><topic>Cyclin-dependent kinase 4</topic><topic>Diabetes</topic><topic>Ethics</topic><topic>Female</topic><topic>G1 phase</topic><topic>G1 Phase - drug effects</topic><topic>G1 Phase - genetics</topic><topic>Gastric cancer</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Medicine</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Pathogens</topic><topic>Pathways</topic><topic>Regulators</topic><topic>Resveratrol</topic><topic>RNA, Small Interfering - 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In this study, we examined the effects and the underlying mechanisms of resveratrol on gastric cancer. We found that resveratrol inhibited the proliferation of gastric cancer cells in a dose-dependent manner. At the concentration of 25 and 50 µM, resveratrol inhibited the cell viability and diminished the clonogenic potential of gastric cancer cells. Resveratrol treatment arrested gastric cancer cells in the G1 phase and led to senescence instead of apoptosis. Regulators of the cell cycle and senescence pathways, including cyclin D1, cyclin-dependent kinase (CDK4 and 6), p21 and p16, were dysregulated by resveratrol treatment. The inhibitory effects of resveratrol on gastric cancer were also verified in vivo using a nude mice xenograft model. Resveratrol (40 mg/kg/d) exerted inhibitory activities on gastric cancer development and significantly decreased the fractions of Ki67-positive cells in the tumor specimens from the nude mice. After resveratrol treatment, the induction of senescence and the changes in the expression of the regulators involved in the cell cycle and senescence pathways were similar to what we observed in vitro. However, the depletion of Sirtuin (Sirt)1 reversed the above-described effects of resveratrol both in vitro and in vivo. Our data suggest that resveratrol inhibits gastric cancer in a Sirt1-dependent manner and provide detailed evidence for the possibility of applying resveratrol in gastric cancer prevention and therapy.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24278101</pmid><doi>10.1371/journal.pone.0070627</doi><tpages>e70627</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2013-11, Vol.8 (11), p.e70627-e70627 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1460505127 |
| source | MEDLINE; Public Library of Science; Full-Text Journals in Chemistry (Open access); PubMed Central; Directory of Open Access Journals; EZB Electronic Journals Library |
| subjects | Animals Anticancer properties Antitumor activity Apoptosis Apoptosis - drug effects Apoptosis - genetics Biochemistry Biology Blotting, Western Breast cancer Cancer Cancer prevention Cancer therapies Cancer treatment Cell cycle Cell Cycle - drug effects Cell Cycle - genetics Cell growth Cell Line, Tumor Cell proliferation Cell Survival - drug effects Cell Survival - genetics Cellular Senescence - drug effects Cellular Senescence - genetics Cyclin D1 Cyclin-dependent kinase 4 Diabetes Ethics Female G1 phase G1 Phase - drug effects G1 Phase - genetics Gastric cancer Health aspects Humans Immunohistochemistry Medicine Mice Mice, Inbred BALB C Mice, Nude Pathogens Pathways Regulators Resveratrol RNA, Small Interfering - genetics Senescence SIRT1 protein Sirtuin 1 - genetics Sirtuin 1 - metabolism Stilbenes - pharmacology Stilbenes - therapeutic use Stomach cancer Stomach Neoplasms - drug therapy Stomach Neoplasms - genetics Stomach Neoplasms - metabolism Xenograft Model Antitumor Assays Xenografts |
| title | Resveratrol inhibits the growth of gastric cancer by inducing G1 phase arrest and senescence in a Sirt1-dependent manner |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-22T18%3A09%3A10IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Resveratrol%20inhibits%20the%20growth%20of%20gastric%20cancer%20by%20inducing%20G1%20phase%20arrest%20and%20senescence%20in%20a%20Sirt1-dependent%20manner&rft.jtitle=PloS%20one&rft.au=Yang,%20Qing&rft.date=2013-11-21&rft.volume=8&rft.issue=11&rft.spage=e70627&rft.epage=e70627&rft.pages=e70627-e70627&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0070627&rft_dat=%3Cgale_plos_%3EA478172032%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1460505127&rft_id=info:pmid/24278101&rft_galeid=A478172032&rft_doaj_id=oai_doaj_org_article_e0554fba85b14a6eab011311679913e9&rfr_iscdi=true |