Survivin Down-regulation by α-Santalol Is Not Mediated Through PI3K-AKT Pathway in Human Breast Cancer Cells
α-Santalol, a terpenoid found in sandalwood oil, has been shown to inhibit cancer cell growth in vitro by inducing apoptosis. This study was performed to investigate the anticancer properties of α-santalol associated with the induction of apoptosis in cultured MCF-7 [estrogen receptor (ER)-positive,...
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| Veröffentlicht in: | Anticancer research 2015-10, Vol.35 (10), p.5353-5357 |
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| creator | Bommareddy, Ajay Crisamore, Karryn Fillman, Sarah Brozena, Sarah Steigerwalt, James Landis, Terra Vanwert, Adam L Dwivedi, Chandradhar |
| description | α-Santalol, a terpenoid found in sandalwood oil, has been shown to inhibit cancer cell growth in vitro by inducing apoptosis. This study was performed to investigate the anticancer properties of α-santalol associated with the induction of apoptosis in cultured MCF-7 [estrogen receptor (ER)-positive, and wild-type p53)] and MDA-MB-231 (ER-negative and mutant p53) breast cancer cells.
Expression of major proteins examined in the study were determined using a standard western blot protocol and analyzed by LICOR-Odyssey infra-red scanner. Total protein levels of survivin were confirmed by survivin enzyme-linked immunosorbent assay (ELISA) kit. Cell viability was assessed by the trypan blue dye exclusion assay, and caspase-3 activity was determined by caspase-3 (active) ELISA kit.
Treatment of breast cancer cells for 6 and 9 h with α-santalol (20, and 40 μM) resulted in statistically significant concentration-dependent down-regulation of survivin. Phosphorylated protein kinase B (pAKT) levels were found to be slightly up-regulated despite the down-regulation of survivin. Pharmacological inhibition of the phosphoinositide 3-kinase - protein kinase B (PI3K-AKT) pathway did not result in a synergistic/additive increase in cell death or caspase-3 activity caused by α-santalol.
The study reveals that survivin down-regulation by α-santalol in breast cancer cells is not mediated through the PI3K-AKT pathway. |
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Expression of major proteins examined in the study were determined using a standard western blot protocol and analyzed by LICOR-Odyssey infra-red scanner. Total protein levels of survivin were confirmed by survivin enzyme-linked immunosorbent assay (ELISA) kit. Cell viability was assessed by the trypan blue dye exclusion assay, and caspase-3 activity was determined by caspase-3 (active) ELISA kit.
Treatment of breast cancer cells for 6 and 9 h with α-santalol (20, and 40 μM) resulted in statistically significant concentration-dependent down-regulation of survivin. Phosphorylated protein kinase B (pAKT) levels were found to be slightly up-regulated despite the down-regulation of survivin. Pharmacological inhibition of the phosphoinositide 3-kinase - protein kinase B (PI3K-AKT) pathway did not result in a synergistic/additive increase in cell death or caspase-3 activity caused by α-santalol.
The study reveals that survivin down-regulation by α-santalol in breast cancer cells is not mediated through the PI3K-AKT pathway.</description><identifier>EISSN: 1791-7530</identifier><identifier>PMID: 26408696</identifier><language>eng</language><publisher>Greece</publisher><subject>Antineoplastic Agents - pharmacology ; Apoptosis ; Breast Neoplasms - drug therapy ; Breast Neoplasms - metabolism ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Chromones - pharmacology ; Down-Regulation ; Female ; Gene Expression Regulation, Neoplastic - drug effects ; Humans ; Inhibitor of Apoptosis Proteins - metabolism ; MAP Kinase Signaling System - drug effects ; MCF-7 Cells ; Morpholines - pharmacology ; Sesquiterpenes - pharmacology</subject><ispartof>Anticancer research, 2015-10, Vol.35 (10), p.5353-5357</ispartof><rights>Copyright© 2015 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26408696$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bommareddy, Ajay</creatorcontrib><creatorcontrib>Crisamore, Karryn</creatorcontrib><creatorcontrib>Fillman, Sarah</creatorcontrib><creatorcontrib>Brozena, Sarah</creatorcontrib><creatorcontrib>Steigerwalt, James</creatorcontrib><creatorcontrib>Landis, Terra</creatorcontrib><creatorcontrib>Vanwert, Adam L</creatorcontrib><creatorcontrib>Dwivedi, Chandradhar</creatorcontrib><title>Survivin Down-regulation by α-Santalol Is Not Mediated Through PI3K-AKT Pathway in Human Breast Cancer Cells</title><title>Anticancer research</title><addtitle>Anticancer Res</addtitle><description>α-Santalol, a terpenoid found in sandalwood oil, has been shown to inhibit cancer cell growth in vitro by inducing apoptosis. This study was performed to investigate the anticancer properties of α-santalol associated with the induction of apoptosis in cultured MCF-7 [estrogen receptor (ER)-positive, and wild-type p53)] and MDA-MB-231 (ER-negative and mutant p53) breast cancer cells.
Expression of major proteins examined in the study were determined using a standard western blot protocol and analyzed by LICOR-Odyssey infra-red scanner. Total protein levels of survivin were confirmed by survivin enzyme-linked immunosorbent assay (ELISA) kit. Cell viability was assessed by the trypan blue dye exclusion assay, and caspase-3 activity was determined by caspase-3 (active) ELISA kit.
Treatment of breast cancer cells for 6 and 9 h with α-santalol (20, and 40 μM) resulted in statistically significant concentration-dependent down-regulation of survivin. Phosphorylated protein kinase B (pAKT) levels were found to be slightly up-regulated despite the down-regulation of survivin. Pharmacological inhibition of the phosphoinositide 3-kinase - protein kinase B (PI3K-AKT) pathway did not result in a synergistic/additive increase in cell death or caspase-3 activity caused by α-santalol.
The study reveals that survivin down-regulation by α-santalol in breast cancer cells is not mediated through the PI3K-AKT pathway.</description><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Chromones - pharmacology</subject><subject>Down-Regulation</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Humans</subject><subject>Inhibitor of Apoptosis Proteins - metabolism</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>MCF-7 Cells</subject><subject>Morpholines - pharmacology</subject><subject>Sesquiterpenes - pharmacology</subject><issn>1791-7530</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1kEtOwzAURSMkREthC8hDJpb8SexkWMKnUQtUahlHL4ndBiV2sZ1WXRYbYU1Uoozu5Ojo6F5EYyozimXCySi69v6TECGylF9FIyZikopMjKN-Nbh9u28NerQHg53aDB2E1hpUHdHPN16BCdDZDhUevdmAXlXTQlANWm-dHTZbtCz4HE_na7SEsD3AEZ1Us6EHgx6cAh9QDqZWDuWq6_xNdKmh8-r2vJPo4_lpnc_w4v2lyKcLvGOUBpwCS2qtGOiaqJSRuGG0SVVFdKwBdFJTClKwWCaiqbIq0TIhuqIppUTyRqZ8Et3_eXfOfg3Kh7JvfX0qAKPs4Esqqcg4zwQ9oXdndKh61ZQ71_bgjuX_RfwXL6Fhww</recordid><startdate>201510</startdate><enddate>201510</enddate><creator>Bommareddy, Ajay</creator><creator>Crisamore, Karryn</creator><creator>Fillman, Sarah</creator><creator>Brozena, Sarah</creator><creator>Steigerwalt, James</creator><creator>Landis, Terra</creator><creator>Vanwert, Adam L</creator><creator>Dwivedi, Chandradhar</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>201510</creationdate><title>Survivin Down-regulation by α-Santalol Is Not Mediated Through PI3K-AKT Pathway in Human Breast Cancer Cells</title><author>Bommareddy, Ajay ; Crisamore, Karryn ; Fillman, Sarah ; Brozena, Sarah ; Steigerwalt, James ; Landis, Terra ; Vanwert, Adam L ; Dwivedi, Chandradhar</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p211t-8a25cfe2afc0e8204d21d8eb0f4faaf5c11a7624756db9b5f750fb1811073d783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Antineoplastic Agents - pharmacology</topic><topic>Apoptosis</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - metabolism</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Chromones - pharmacology</topic><topic>Down-Regulation</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Humans</topic><topic>Inhibitor of Apoptosis Proteins - metabolism</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>MCF-7 Cells</topic><topic>Morpholines - pharmacology</topic><topic>Sesquiterpenes - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bommareddy, Ajay</creatorcontrib><creatorcontrib>Crisamore, Karryn</creatorcontrib><creatorcontrib>Fillman, Sarah</creatorcontrib><creatorcontrib>Brozena, Sarah</creatorcontrib><creatorcontrib>Steigerwalt, James</creatorcontrib><creatorcontrib>Landis, Terra</creatorcontrib><creatorcontrib>Vanwert, Adam L</creatorcontrib><creatorcontrib>Dwivedi, Chandradhar</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Anticancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bommareddy, Ajay</au><au>Crisamore, Karryn</au><au>Fillman, Sarah</au><au>Brozena, Sarah</au><au>Steigerwalt, James</au><au>Landis, Terra</au><au>Vanwert, Adam L</au><au>Dwivedi, Chandradhar</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Survivin Down-regulation by α-Santalol Is Not Mediated Through PI3K-AKT Pathway in Human Breast Cancer Cells</atitle><jtitle>Anticancer research</jtitle><addtitle>Anticancer Res</addtitle><date>2015-10</date><risdate>2015</risdate><volume>35</volume><issue>10</issue><spage>5353</spage><epage>5357</epage><pages>5353-5357</pages><eissn>1791-7530</eissn><abstract>α-Santalol, a terpenoid found in sandalwood oil, has been shown to inhibit cancer cell growth in vitro by inducing apoptosis. This study was performed to investigate the anticancer properties of α-santalol associated with the induction of apoptosis in cultured MCF-7 [estrogen receptor (ER)-positive, and wild-type p53)] and MDA-MB-231 (ER-negative and mutant p53) breast cancer cells.
Expression of major proteins examined in the study were determined using a standard western blot protocol and analyzed by LICOR-Odyssey infra-red scanner. Total protein levels of survivin were confirmed by survivin enzyme-linked immunosorbent assay (ELISA) kit. Cell viability was assessed by the trypan blue dye exclusion assay, and caspase-3 activity was determined by caspase-3 (active) ELISA kit.
Treatment of breast cancer cells for 6 and 9 h with α-santalol (20, and 40 μM) resulted in statistically significant concentration-dependent down-regulation of survivin. Phosphorylated protein kinase B (pAKT) levels were found to be slightly up-regulated despite the down-regulation of survivin. Pharmacological inhibition of the phosphoinositide 3-kinase - protein kinase B (PI3K-AKT) pathway did not result in a synergistic/additive increase in cell death or caspase-3 activity caused by α-santalol.
The study reveals that survivin down-regulation by α-santalol in breast cancer cells is not mediated through the PI3K-AKT pathway.</abstract><cop>Greece</cop><pmid>26408696</pmid><tpages>5</tpages></addata></record> |
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| ispartof | Anticancer research, 2015-10, Vol.35 (10), p.5353-5357 |
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| subjects | Antineoplastic Agents - pharmacology Apoptosis Breast Neoplasms - drug therapy Breast Neoplasms - metabolism Cell Line, Tumor Cell Proliferation - drug effects Chromones - pharmacology Down-Regulation Female Gene Expression Regulation, Neoplastic - drug effects Humans Inhibitor of Apoptosis Proteins - metabolism MAP Kinase Signaling System - drug effects MCF-7 Cells Morpholines - pharmacology Sesquiterpenes - pharmacology |
| title | Survivin Down-regulation by α-Santalol Is Not Mediated Through PI3K-AKT Pathway in Human Breast Cancer Cells |
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