Epigallocatechin gallate (EGCG) suppresses growth and tumorigenicity in breast cancer cells by downregulation of miR-25
The aim of the present study was to investigate the anticancer effects and potential mechanisms of polyphenol epigallocatechin-3-gallate (EGCG) on breast cancer MCF-7 cells in vitro and in vivo. Our results showed that EGCG significantly inhibited MCF-7 cell viability in a time- and dose-dependent m...
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| Veröffentlicht in: | Bioengineered 2019-01, Vol.10 (1), p.374-382 |
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| creator | Zan, Lingling Chen, Qingfeng Zhang, Lei Li, Xiaona |
| description | The aim of the present study was to investigate the anticancer effects and potential mechanisms of polyphenol epigallocatechin-3-gallate (EGCG) on breast cancer MCF-7 cells in vitro and in vivo. Our results showed that EGCG significantly inhibited MCF-7 cell viability in a time- and dose-dependent manner. Flow cytometry analysis indicated that EGCG induced apoptosis and disrupted cell cycle progression at G2/M phase. Moreover, EGCG inhibited miR-25 expression and increased PARP, pro-caspase-3 and pro-caspase-9 at protein levels. Restoration of miR-25 inhibited EGCG-induced cell apoptosis. Furthermore, EGCG suppressed tumor growth in vivo by downregulating the expression of miR-25 and proteins associated with apoptosis, which was further confirmed by a reduction of Ki-67 and increase of pro-apoptotic PARP expression as determined by immunohistochemistry staining. These findings indicate that EGCG possesses chemopreventive potential in breast cancer which may serve as a promising anticancer agent for clinical applications. |
| doi_str_mv | 10.1080/21655979.2019.1657327 |
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Our results showed that EGCG significantly inhibited MCF-7 cell viability in a time- and dose-dependent manner. Flow cytometry analysis indicated that EGCG induced apoptosis and disrupted cell cycle progression at G2/M phase. Moreover, EGCG inhibited miR-25 expression and increased PARP, pro-caspase-3 and pro-caspase-9 at protein levels. Restoration of miR-25 inhibited EGCG-induced cell apoptosis. Furthermore, EGCG suppressed tumor growth in vivo by downregulating the expression of miR-25 and proteins associated with apoptosis, which was further confirmed by a reduction of Ki-67 and increase of pro-apoptotic PARP expression as determined by immunohistochemistry staining. These findings indicate that EGCG possesses chemopreventive potential in breast cancer which may serve as a promising anticancer agent for clinical applications.</description><identifier>ISSN: 2165-5979</identifier><identifier>EISSN: 2165-5987</identifier><identifier>DOI: 10.1080/21655979.2019.1657327</identifier><identifier>PMID: 31431131</identifier><language>eng</language><publisher>United States: Taylor & Francis</publisher><subject>Animals ; Antineoplastic Agents, Phytogenic - pharmacology ; apoptosis ; Apoptosis - drug effects ; Apoptosis - genetics ; breast cancer ; Breast Neoplasms - drug therapy ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Caspase 3 - genetics ; Caspase 3 - metabolism ; Caspase 9 - genetics ; Caspase 9 - metabolism ; Catechin - analogs & derivatives ; Catechin - pharmacology ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Dose-Response Relationship, Drug ; Female ; G2 Phase Cell Cycle Checkpoints - drug effects ; G2 Phase Cell Cycle Checkpoints - genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Ki-67 Antigen - genetics ; Ki-67 Antigen - metabolism ; MCF-7 Cells ; Mice ; Mice, SCID ; MicroRNAs - antagonists & inhibitors ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Poly(ADP-ribose) Polymerases - genetics ; Poly(ADP-ribose) Polymerases - metabolism ; Polyphenol epigallocatechin-3-gallate ; proliferation ; Research Paper ; Signal Transduction ; Tumor Burden - drug effects ; Xenograft Model Antitumor Assays</subject><ispartof>Bioengineered, 2019-01, Vol.10 (1), p.374-382</ispartof><rights>2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. 2019</rights><rights>2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. 2019 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c534t-51ff9d98b3ecd45691bf577e9ec2baf8845f625e7dfe53451526cba240b5e4853</citedby><cites>FETCH-LOGICAL-c534t-51ff9d98b3ecd45691bf577e9ec2baf8845f625e7dfe53451526cba240b5e4853</cites><orcidid>0000-0002-8458-4036</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6738446/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6738446/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,883,27485,27907,27908,53774,53776,59124,59125</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31431131$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zan, Lingling</creatorcontrib><creatorcontrib>Chen, Qingfeng</creatorcontrib><creatorcontrib>Zhang, Lei</creatorcontrib><creatorcontrib>Li, Xiaona</creatorcontrib><title>Epigallocatechin gallate (EGCG) suppresses growth and tumorigenicity in breast cancer cells by downregulation of miR-25</title><title>Bioengineered</title><addtitle>Bioengineered</addtitle><description>The aim of the present study was to investigate the anticancer effects and potential mechanisms of polyphenol epigallocatechin-3-gallate (EGCG) on breast cancer MCF-7 cells in vitro and in vivo. Our results showed that EGCG significantly inhibited MCF-7 cell viability in a time- and dose-dependent manner. Flow cytometry analysis indicated that EGCG induced apoptosis and disrupted cell cycle progression at G2/M phase. Moreover, EGCG inhibited miR-25 expression and increased PARP, pro-caspase-3 and pro-caspase-9 at protein levels. Restoration of miR-25 inhibited EGCG-induced cell apoptosis. Furthermore, EGCG suppressed tumor growth in vivo by downregulating the expression of miR-25 and proteins associated with apoptosis, which was further confirmed by a reduction of Ki-67 and increase of pro-apoptotic PARP expression as determined by immunohistochemistry staining. These findings indicate that EGCG possesses chemopreventive potential in breast cancer which may serve as a promising anticancer agent for clinical applications.</description><subject>Animals</subject><subject>Antineoplastic Agents, Phytogenic - pharmacology</subject><subject>apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>breast cancer</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Caspase 3 - genetics</subject><subject>Caspase 3 - metabolism</subject><subject>Caspase 9 - genetics</subject><subject>Caspase 9 - metabolism</subject><subject>Catechin - analogs & derivatives</subject><subject>Catechin - pharmacology</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Dose-Response Relationship, Drug</subject><subject>Female</subject><subject>G2 Phase Cell Cycle Checkpoints - drug effects</subject><subject>G2 Phase Cell Cycle Checkpoints - genetics</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Ki-67 Antigen - genetics</subject><subject>Ki-67 Antigen - metabolism</subject><subject>MCF-7 Cells</subject><subject>Mice</subject><subject>Mice, SCID</subject><subject>MicroRNAs - antagonists & inhibitors</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Poly(ADP-ribose) Polymerases - genetics</subject><subject>Poly(ADP-ribose) Polymerases - metabolism</subject><subject>Polyphenol epigallocatechin-3-gallate</subject><subject>proliferation</subject><subject>Research Paper</subject><subject>Signal Transduction</subject><subject>Tumor Burden - drug effects</subject><subject>Xenograft Model Antitumor Assays</subject><issn>2165-5979</issn><issn>2165-5987</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>0YH</sourceid><sourceid>EIF</sourceid><recordid>eNp9kVGP1CAUhRujcTfr_gQNj-tDR6BQyovRTMbRZBMTo8-E0ksH00KF1sn8e2lmdqIvPnEvfOdc4BTFa4I3BDf4HSU151LIDcVEbnIjKiqeFbfrfsllI55fayFvivuUfmKMCa4YF83L4qYirCKkIrfFcTe5Xg9DMHoGc3AerV2u0cNuv92_RWmZpggpQUJ9DMf5gLTv0LyMIboevDNuPqEsayPoNCOjvYGIDAxDQu0JdeHoI_RLtnTBo2DR6L6VlL8qXlg9JLi_rHfFj0-779vP5ePX_Zftx8fS8IrNJSfWyk42bQWmY7yWpLVcCJBgaKtt0zBua8pBdBaygBNOa9NqynDLgTW8uiven32npR2hM-DnqAc1RTfqeFJBO_XviXcH1YffqhZVw1idDR4uBjH8WiDNanRpfZ72EJakKG0okxWhK8rPqIkhpQj2OoZgteamnnJTa27qklvWvfn7jlfVU0oZ-HAGnLchjvoY4tCpWZ-GEG3MP-5Shv874w8iram2</recordid><startdate>20190101</startdate><enddate>20190101</enddate><creator>Zan, Lingling</creator><creator>Chen, Qingfeng</creator><creator>Zhang, Lei</creator><creator>Li, Xiaona</creator><general>Taylor & Francis</general><scope>0YH</scope><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>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-8458-4036</orcidid></search><sort><creationdate>20190101</creationdate><title>Epigallocatechin gallate (EGCG) suppresses growth and tumorigenicity in breast cancer cells by downregulation of miR-25</title><author>Zan, Lingling ; Chen, Qingfeng ; Zhang, Lei ; Li, Xiaona</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c534t-51ff9d98b3ecd45691bf577e9ec2baf8845f625e7dfe53451526cba240b5e4853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Antineoplastic Agents, Phytogenic - pharmacology</topic><topic>apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - genetics</topic><topic>breast cancer</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Caspase 3 - genetics</topic><topic>Caspase 3 - metabolism</topic><topic>Caspase 9 - genetics</topic><topic>Caspase 9 - metabolism</topic><topic>Catechin - analogs & derivatives</topic><topic>Catechin - pharmacology</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Dose-Response Relationship, Drug</topic><topic>Female</topic><topic>G2 Phase Cell Cycle Checkpoints - drug effects</topic><topic>G2 Phase Cell Cycle Checkpoints - genetics</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Ki-67 Antigen - genetics</topic><topic>Ki-67 Antigen - metabolism</topic><topic>MCF-7 Cells</topic><topic>Mice</topic><topic>Mice, SCID</topic><topic>MicroRNAs - antagonists & inhibitors</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Poly(ADP-ribose) Polymerases - genetics</topic><topic>Poly(ADP-ribose) Polymerases - metabolism</topic><topic>Polyphenol epigallocatechin-3-gallate</topic><topic>proliferation</topic><topic>Research Paper</topic><topic>Signal Transduction</topic><topic>Tumor Burden - drug effects</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zan, Lingling</creatorcontrib><creatorcontrib>Chen, Qingfeng</creatorcontrib><creatorcontrib>Zhang, Lei</creatorcontrib><creatorcontrib>Li, Xiaona</creatorcontrib><collection>Taylor & Francis Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Bioengineered</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zan, Lingling</au><au>Chen, Qingfeng</au><au>Zhang, Lei</au><au>Li, Xiaona</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Epigallocatechin gallate (EGCG) suppresses growth and tumorigenicity in breast cancer cells by downregulation of miR-25</atitle><jtitle>Bioengineered</jtitle><addtitle>Bioengineered</addtitle><date>2019-01-01</date><risdate>2019</risdate><volume>10</volume><issue>1</issue><spage>374</spage><epage>382</epage><pages>374-382</pages><issn>2165-5979</issn><eissn>2165-5987</eissn><abstract>The aim of the present study was to investigate the anticancer effects and potential mechanisms of polyphenol epigallocatechin-3-gallate (EGCG) on breast cancer MCF-7 cells in vitro and in vivo. Our results showed that EGCG significantly inhibited MCF-7 cell viability in a time- and dose-dependent manner. Flow cytometry analysis indicated that EGCG induced apoptosis and disrupted cell cycle progression at G2/M phase. Moreover, EGCG inhibited miR-25 expression and increased PARP, pro-caspase-3 and pro-caspase-9 at protein levels. Restoration of miR-25 inhibited EGCG-induced cell apoptosis. Furthermore, EGCG suppressed tumor growth in vivo by downregulating the expression of miR-25 and proteins associated with apoptosis, which was further confirmed by a reduction of Ki-67 and increase of pro-apoptotic PARP expression as determined by immunohistochemistry staining. These findings indicate that EGCG possesses chemopreventive potential in breast cancer which may serve as a promising anticancer agent for clinical applications.</abstract><cop>United States</cop><pub>Taylor & Francis</pub><pmid>31431131</pmid><doi>10.1080/21655979.2019.1657327</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-8458-4036</orcidid><oa>free_for_read</oa></addata></record> |
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| source | Taylor & Francis Open Access; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Animals Antineoplastic Agents, Phytogenic - pharmacology apoptosis Apoptosis - drug effects Apoptosis - genetics breast cancer Breast Neoplasms - drug therapy Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Caspase 3 - genetics Caspase 3 - metabolism Caspase 9 - genetics Caspase 9 - metabolism Catechin - analogs & derivatives Catechin - pharmacology Cell Proliferation - drug effects Cell Survival - drug effects Dose-Response Relationship, Drug Female G2 Phase Cell Cycle Checkpoints - drug effects G2 Phase Cell Cycle Checkpoints - genetics Gene Expression Regulation, Neoplastic Humans Ki-67 Antigen - genetics Ki-67 Antigen - metabolism MCF-7 Cells Mice Mice, SCID MicroRNAs - antagonists & inhibitors MicroRNAs - genetics MicroRNAs - metabolism Poly(ADP-ribose) Polymerases - genetics Poly(ADP-ribose) Polymerases - metabolism Polyphenol epigallocatechin-3-gallate proliferation Research Paper Signal Transduction Tumor Burden - drug effects Xenograft Model Antitumor Assays |
| title | Epigallocatechin gallate (EGCG) suppresses growth and tumorigenicity in breast cancer cells by downregulation of miR-25 |
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