Silymarin inhibits the progression of Ehrlich solid tumor via targeting molecular pathways of cell death, proliferation, angiogenesis, and metastasis in female mice
Background Plant-derived phytochemicals have been reported to exert anticancer activity. This study investigated the antitumor role of silymarin ( Silybum marianum ) (SMN) and its molecular targets in Ehrlich solid tumor xenografts in vivo. Methods and results Female Swiss albino mice were divided i...
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| Veröffentlicht in: | Molecular biology reports 2022-06, Vol.49 (6), p.4659-4671 |
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| creator | Amer, Maggie E. Amer, Maher A. Othman, Azza I. Elsayed, Doaa A. El-Missiry, Mohamed Amr Ammar, Omar A. |
| description | Background
Plant-derived phytochemicals have been reported to exert anticancer activity. This study investigated the antitumor role of silymarin (
Silybum marianum
) (SMN) and its molecular targets in Ehrlich solid tumor xenografts in vivo.
Methods and results
Female Swiss albino mice were divided into three groups (of five animals each) that were engrafted with Ehrlich tumor (ET) cells with or without SMN treatment. The 3rd groups treated with DMSO only vehicle control group. A significant reduction in animal body mass and tumor volume/weight were observed in xenografted mice treated with SMN. SMN modulated oxidative stress in tumors while enhancing the antioxidant levels in mouse serum. SMN activated both mitochondrial and death receptor-related apoptosis pathways and induced cell cycle arrest, marked by a significant downregulation of cyclin D1 in SMN-treated tumors. Significant decreases in RNA content and protein expression levels of Ki-67 and proliferating cell nuclear antigen were observed in ET cells. Additionally, SMN downregulated vascular endothelial growth factor and nuclear factor-kappa B levels indicating anti-angiogenesis activity of this agent. SMN upregulated the expression of E-cadherin in tumor tissue suggesting, that SMN has potential ability to inhibit metastasis. Tumor tissue from SMN-treated animals showed a remarkable degeneration and reduction in the neoplastic cell density.
Conclusions
The anticancer effect was associated with apparent apoptosis in neoplastic cells with abundance of multifocal necrotic areas. SMN was found to inhibit ET growth via enhancing apoptosis, inhibition of cell division and reduction in angiogenesis in vivo
.
Graphical abstract
Hypothetical scheme of SMN antitumor effects (mechanism of signaling) in solid ET in vivo. SMN anticancer effect may be mediated by molecular mediators that affect proliferation, cell cycle activity, apoptotic pathways, angiogenesis, and metastasis. |
| doi_str_mv | 10.1007/s11033-022-07315-2 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2640995887</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2640995887</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-81c12c59eba35c467eaf3e3fbaf077525635c5784a43caac73dcb09da2f7ee683</originalsourceid><addsrcrecordid>eNp9kc1u1TAQhS0EopfCC7BAltiwaMA_cZwsUVUKUqUuWtbRxJkkrpz4YjtF9314UJzeAhKLSpYsj785Pp5DyFvOPnLG9KfIOZOyYEIUTEuuCvGM7LjSsigbXT8nOyYZL8pa8RPyKsY7xljJtXpJTqSSTAmhd-TXjXWHGYJdqF0m29kUaZqQ7oMfA8Zo_UL9QC-m4KyZaPTO9jStsw_03gJNEEZMdhnp7B2a1UGge0jTTzjErc-gc7THXDnbJJ0dMEDKomcUltH6EReMNm6nns6YIOZlY_ZCB5zBIZ2twdfkxQAu4pvH_ZR8_3Jxe_61uLq-_Hb--aowUqtU1NxwYVSDHUhlykojDBLl0MHAtFZCVbmsdF1CKQ2A0bI3HWt6EINGrGp5Sj4cdbPVHyvG1M42bl-ABf0aW1GVrGlUXeuMvv8PvfNrWLK7TNWqzsNtqkyJI2WCjzHg0O6DzdM-tJy1W4btMcM2Z9g-ZNiK3PTuUXrtZuz_tvwJLQPyCMR8tYwY_r39hOxvNoWqwA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2685822796</pqid></control><display><type>article</type><title>Silymarin inhibits the progression of Ehrlich solid tumor via targeting molecular pathways of cell death, proliferation, angiogenesis, and metastasis in female mice</title><source>SpringerNature Journals</source><creator>Amer, Maggie E. ; Amer, Maher A. ; Othman, Azza I. ; Elsayed, Doaa A. ; El-Missiry, Mohamed Amr ; Ammar, Omar A.</creator><creatorcontrib>Amer, Maggie E. ; Amer, Maher A. ; Othman, Azza I. ; Elsayed, Doaa A. ; El-Missiry, Mohamed Amr ; Ammar, Omar A.</creatorcontrib><description>Background
Plant-derived phytochemicals have been reported to exert anticancer activity. This study investigated the antitumor role of silymarin (
Silybum marianum
) (SMN) and its molecular targets in Ehrlich solid tumor xenografts in vivo.
Methods and results
Female Swiss albino mice were divided into three groups (of five animals each) that were engrafted with Ehrlich tumor (ET) cells with or without SMN treatment. The 3rd groups treated with DMSO only vehicle control group. A significant reduction in animal body mass and tumor volume/weight were observed in xenografted mice treated with SMN. SMN modulated oxidative stress in tumors while enhancing the antioxidant levels in mouse serum. SMN activated both mitochondrial and death receptor-related apoptosis pathways and induced cell cycle arrest, marked by a significant downregulation of cyclin D1 in SMN-treated tumors. Significant decreases in RNA content and protein expression levels of Ki-67 and proliferating cell nuclear antigen were observed in ET cells. Additionally, SMN downregulated vascular endothelial growth factor and nuclear factor-kappa B levels indicating anti-angiogenesis activity of this agent. SMN upregulated the expression of E-cadherin in tumor tissue suggesting, that SMN has potential ability to inhibit metastasis. Tumor tissue from SMN-treated animals showed a remarkable degeneration and reduction in the neoplastic cell density.
Conclusions
The anticancer effect was associated with apparent apoptosis in neoplastic cells with abundance of multifocal necrotic areas. SMN was found to inhibit ET growth via enhancing apoptosis, inhibition of cell division and reduction in angiogenesis in vivo
.
Graphical abstract
Hypothetical scheme of SMN antitumor effects (mechanism of signaling) in solid ET in vivo. SMN anticancer effect may be mediated by molecular mediators that affect proliferation, cell cycle activity, apoptotic pathways, angiogenesis, and metastasis.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-022-07315-2</identifier><identifier>PMID: 35305227</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Angiogenesis ; Animal Anatomy ; Animal Biochemistry ; Antioxidants ; Antitumor activity ; Apoptosis ; Biomedical and Life Sciences ; Body mass ; Cancer ; Cell cycle ; Cell death ; Cell density ; Cell division ; Cyclin D1 ; Degeneration ; E-cadherin ; Histology ; Life Sciences ; Metastases ; Metastasis ; Mitochondria ; Morphology ; NF-κB protein ; Original Article ; Oxidative stress ; Plants ; Proliferating cell nuclear antigen ; Silymarin ; Solid tumors ; Tumors ; Vascular endothelial growth factor ; Xenografts</subject><ispartof>Molecular biology reports, 2022-06, Vol.49 (6), p.4659-4671</ispartof><rights>The Author(s), under exclusive licence to Springer Nature B.V. 2022</rights><rights>2022. The Author(s), under exclusive licence to Springer Nature B.V.</rights><rights>The Author(s), under exclusive licence to Springer Nature B.V. 2022.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-81c12c59eba35c467eaf3e3fbaf077525635c5784a43caac73dcb09da2f7ee683</citedby><cites>FETCH-LOGICAL-c375t-81c12c59eba35c467eaf3e3fbaf077525635c5784a43caac73dcb09da2f7ee683</cites><orcidid>0000-0002-4566-0497 ; 0000-0003-2012-9154 ; 0000-0001-9377-6462 ; 0000-0001-8624-1259 ; 0000-0002-9000-6646</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11033-022-07315-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11033-022-07315-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35305227$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Amer, Maggie E.</creatorcontrib><creatorcontrib>Amer, Maher A.</creatorcontrib><creatorcontrib>Othman, Azza I.</creatorcontrib><creatorcontrib>Elsayed, Doaa A.</creatorcontrib><creatorcontrib>El-Missiry, Mohamed Amr</creatorcontrib><creatorcontrib>Ammar, Omar A.</creatorcontrib><title>Silymarin inhibits the progression of Ehrlich solid tumor via targeting molecular pathways of cell death, proliferation, angiogenesis, and metastasis in female mice</title><title>Molecular biology reports</title><addtitle>Mol Biol Rep</addtitle><addtitle>Mol Biol Rep</addtitle><description>Background
Plant-derived phytochemicals have been reported to exert anticancer activity. This study investigated the antitumor role of silymarin (
Silybum marianum
) (SMN) and its molecular targets in Ehrlich solid tumor xenografts in vivo.
Methods and results
Female Swiss albino mice were divided into three groups (of five animals each) that were engrafted with Ehrlich tumor (ET) cells with or without SMN treatment. The 3rd groups treated with DMSO only vehicle control group. A significant reduction in animal body mass and tumor volume/weight were observed in xenografted mice treated with SMN. SMN modulated oxidative stress in tumors while enhancing the antioxidant levels in mouse serum. SMN activated both mitochondrial and death receptor-related apoptosis pathways and induced cell cycle arrest, marked by a significant downregulation of cyclin D1 in SMN-treated tumors. Significant decreases in RNA content and protein expression levels of Ki-67 and proliferating cell nuclear antigen were observed in ET cells. Additionally, SMN downregulated vascular endothelial growth factor and nuclear factor-kappa B levels indicating anti-angiogenesis activity of this agent. SMN upregulated the expression of E-cadherin in tumor tissue suggesting, that SMN has potential ability to inhibit metastasis. Tumor tissue from SMN-treated animals showed a remarkable degeneration and reduction in the neoplastic cell density.
Conclusions
The anticancer effect was associated with apparent apoptosis in neoplastic cells with abundance of multifocal necrotic areas. SMN was found to inhibit ET growth via enhancing apoptosis, inhibition of cell division and reduction in angiogenesis in vivo
.
Graphical abstract
Hypothetical scheme of SMN antitumor effects (mechanism of signaling) in solid ET in vivo. SMN anticancer effect may be mediated by molecular mediators that affect proliferation, cell cycle activity, apoptotic pathways, angiogenesis, and metastasis.</description><subject>Angiogenesis</subject><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Antioxidants</subject><subject>Antitumor activity</subject><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Body mass</subject><subject>Cancer</subject><subject>Cell cycle</subject><subject>Cell death</subject><subject>Cell density</subject><subject>Cell division</subject><subject>Cyclin D1</subject><subject>Degeneration</subject><subject>E-cadherin</subject><subject>Histology</subject><subject>Life Sciences</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mitochondria</subject><subject>Morphology</subject><subject>NF-κB protein</subject><subject>Original Article</subject><subject>Oxidative stress</subject><subject>Plants</subject><subject>Proliferating cell nuclear antigen</subject><subject>Silymarin</subject><subject>Solid tumors</subject><subject>Tumors</subject><subject>Vascular endothelial growth factor</subject><subject>Xenografts</subject><issn>0301-4851</issn><issn>1573-4978</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kc1u1TAQhS0EopfCC7BAltiwaMA_cZwsUVUKUqUuWtbRxJkkrpz4YjtF9314UJzeAhKLSpYsj785Pp5DyFvOPnLG9KfIOZOyYEIUTEuuCvGM7LjSsigbXT8nOyYZL8pa8RPyKsY7xljJtXpJTqSSTAmhd-TXjXWHGYJdqF0m29kUaZqQ7oMfA8Zo_UL9QC-m4KyZaPTO9jStsw_03gJNEEZMdhnp7B2a1UGge0jTTzjErc-gc7THXDnbJJ0dMEDKomcUltH6EReMNm6nns6YIOZlY_ZCB5zBIZ2twdfkxQAu4pvH_ZR8_3Jxe_61uLq-_Hb--aowUqtU1NxwYVSDHUhlykojDBLl0MHAtFZCVbmsdF1CKQ2A0bI3HWt6EINGrGp5Sj4cdbPVHyvG1M42bl-ABf0aW1GVrGlUXeuMvv8PvfNrWLK7TNWqzsNtqkyJI2WCjzHg0O6DzdM-tJy1W4btMcM2Z9g-ZNiK3PTuUXrtZuz_tvwJLQPyCMR8tYwY_r39hOxvNoWqwA</recordid><startdate>20220601</startdate><enddate>20220601</enddate><creator>Amer, Maggie E.</creator><creator>Amer, Maher A.</creator><creator>Othman, Azza I.</creator><creator>Elsayed, Doaa A.</creator><creator>El-Missiry, Mohamed Amr</creator><creator>Ammar, Omar A.</creator><general>Springer Netherlands</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4566-0497</orcidid><orcidid>https://orcid.org/0000-0003-2012-9154</orcidid><orcidid>https://orcid.org/0000-0001-9377-6462</orcidid><orcidid>https://orcid.org/0000-0001-8624-1259</orcidid><orcidid>https://orcid.org/0000-0002-9000-6646</orcidid></search><sort><creationdate>20220601</creationdate><title>Silymarin inhibits the progression of Ehrlich solid tumor via targeting molecular pathways of cell death, proliferation, angiogenesis, and metastasis in female mice</title><author>Amer, Maggie E. ; Amer, Maher A. ; Othman, Azza I. ; Elsayed, Doaa A. ; El-Missiry, Mohamed Amr ; Ammar, Omar A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-81c12c59eba35c467eaf3e3fbaf077525635c5784a43caac73dcb09da2f7ee683</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Angiogenesis</topic><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Antioxidants</topic><topic>Antitumor activity</topic><topic>Apoptosis</topic><topic>Biomedical and Life Sciences</topic><topic>Body mass</topic><topic>Cancer</topic><topic>Cell cycle</topic><topic>Cell death</topic><topic>Cell density</topic><topic>Cell division</topic><topic>Cyclin D1</topic><topic>Degeneration</topic><topic>E-cadherin</topic><topic>Histology</topic><topic>Life Sciences</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Mitochondria</topic><topic>Morphology</topic><topic>NF-κB protein</topic><topic>Original Article</topic><topic>Oxidative stress</topic><topic>Plants</topic><topic>Proliferating cell nuclear antigen</topic><topic>Silymarin</topic><topic>Solid tumors</topic><topic>Tumors</topic><topic>Vascular endothelial growth factor</topic><topic>Xenografts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Amer, Maggie E.</creatorcontrib><creatorcontrib>Amer, Maher A.</creatorcontrib><creatorcontrib>Othman, Azza I.</creatorcontrib><creatorcontrib>Elsayed, Doaa A.</creatorcontrib><creatorcontrib>El-Missiry, Mohamed Amr</creatorcontrib><creatorcontrib>Ammar, Omar A.</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular biology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Amer, Maggie E.</au><au>Amer, Maher A.</au><au>Othman, Azza I.</au><au>Elsayed, Doaa A.</au><au>El-Missiry, Mohamed Amr</au><au>Ammar, Omar A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Silymarin inhibits the progression of Ehrlich solid tumor via targeting molecular pathways of cell death, proliferation, angiogenesis, and metastasis in female mice</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><addtitle>Mol Biol Rep</addtitle><date>2022-06-01</date><risdate>2022</risdate><volume>49</volume><issue>6</issue><spage>4659</spage><epage>4671</epage><pages>4659-4671</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>Background
Plant-derived phytochemicals have been reported to exert anticancer activity. This study investigated the antitumor role of silymarin (
Silybum marianum
) (SMN) and its molecular targets in Ehrlich solid tumor xenografts in vivo.
Methods and results
Female Swiss albino mice were divided into three groups (of five animals each) that were engrafted with Ehrlich tumor (ET) cells with or without SMN treatment. The 3rd groups treated with DMSO only vehicle control group. A significant reduction in animal body mass and tumor volume/weight were observed in xenografted mice treated with SMN. SMN modulated oxidative stress in tumors while enhancing the antioxidant levels in mouse serum. SMN activated both mitochondrial and death receptor-related apoptosis pathways and induced cell cycle arrest, marked by a significant downregulation of cyclin D1 in SMN-treated tumors. Significant decreases in RNA content and protein expression levels of Ki-67 and proliferating cell nuclear antigen were observed in ET cells. Additionally, SMN downregulated vascular endothelial growth factor and nuclear factor-kappa B levels indicating anti-angiogenesis activity of this agent. SMN upregulated the expression of E-cadherin in tumor tissue suggesting, that SMN has potential ability to inhibit metastasis. Tumor tissue from SMN-treated animals showed a remarkable degeneration and reduction in the neoplastic cell density.
Conclusions
The anticancer effect was associated with apparent apoptosis in neoplastic cells with abundance of multifocal necrotic areas. SMN was found to inhibit ET growth via enhancing apoptosis, inhibition of cell division and reduction in angiogenesis in vivo
.
Graphical abstract
Hypothetical scheme of SMN antitumor effects (mechanism of signaling) in solid ET in vivo. SMN anticancer effect may be mediated by molecular mediators that affect proliferation, cell cycle activity, apoptotic pathways, angiogenesis, and metastasis.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>35305227</pmid><doi>10.1007/s11033-022-07315-2</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-4566-0497</orcidid><orcidid>https://orcid.org/0000-0003-2012-9154</orcidid><orcidid>https://orcid.org/0000-0001-9377-6462</orcidid><orcidid>https://orcid.org/0000-0001-8624-1259</orcidid><orcidid>https://orcid.org/0000-0002-9000-6646</orcidid></addata></record> |
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| ispartof | Molecular biology reports, 2022-06, Vol.49 (6), p.4659-4671 |
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| subjects | Angiogenesis Animal Anatomy Animal Biochemistry Antioxidants Antitumor activity Apoptosis Biomedical and Life Sciences Body mass Cancer Cell cycle Cell death Cell density Cell division Cyclin D1 Degeneration E-cadherin Histology Life Sciences Metastases Metastasis Mitochondria Morphology NF-κB protein Original Article Oxidative stress Plants Proliferating cell nuclear antigen Silymarin Solid tumors Tumors Vascular endothelial growth factor Xenografts |
| title | Silymarin inhibits the progression of Ehrlich solid tumor via targeting molecular pathways of cell death, proliferation, angiogenesis, and metastasis in female mice |
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