Guanylate cyclase activator YC-1 potentiates apoptotic effect of licochalcone A on human epithelial ovarian carcinoma cells via activation of death receptor and mitochondrial pathways
Natural phenol licorice compounds have been shown to induce apoptosis in cancer cells. 3-(5′-Hydroxymethyl-2′-furyl)-1-benzyl indazole (YC-1) may enhance the sensitivity of cancer cells to anticancer drugs. However, the combined effect of licochalcone A and YC-1 on cell death in ovarian cancer cells...
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| Veröffentlicht in: | European journal of pharmacology 2012-05, Vol.683 (1-3), p.54-62 |
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| creator | Lee, Chung Soo Kwak, Sang Won Kim, Yun Jeong Lee, Seon Ae Park, Eon Sob Myung, Soon Chul Kim, Wonyong Lee, Min Sung Lee, Jeong Jae |
| description | Natural phenol licorice compounds have been shown to induce apoptosis in cancer cells. 3-(5′-Hydroxymethyl-2′-furyl)-1-benzyl indazole (YC-1) may enhance the sensitivity of cancer cells to anticancer drugs. However, the combined effect of licochalcone A and YC-1 on cell death in ovarian cancer cells has not been studied. We assessed the combined effect of licochalcone A and YC-1 on apoptosis in human epithelial ovarian carcinoma cell lines in relation to the cell death process. In the OVCAR-3 and SK-OV-3 cell lines, licochalocone A induced a decrease in Bid, Bcl-2, Bcl-xL and survivin protein levels; an increase in Bax levels; loss of the mitochondrial transmembrane potential; cytochrome c release; activation of caspases (-8, -9 and -3); cleavage of PARP-1; and an increase in the tumor suppressor p53 levels. YC-1 enhanced licochalcone A-induced apoptosis-related protein activation, nuclear damage and cell death. These results suggest that YC-1 may potentiate the apoptotic effect of licochalcone A on ovarian carcinoma cell lines by increasing the activation of the caspase-8- and Bid-dependent pathway and the mitochondria-mediated apoptotic pathway, leading to caspase activation. The combination of licochalcone A and YC-1 may confer a benefit in the treatment of human epithelial ovarian adenocarcinoma. |
| doi_str_mv | 10.1016/j.ejphar.2012.03.024 |
| format | Article |
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However, the combined effect of licochalcone A and YC-1 on cell death in ovarian cancer cells has not been studied. We assessed the combined effect of licochalcone A and YC-1 on apoptosis in human epithelial ovarian carcinoma cell lines in relation to the cell death process. In the OVCAR-3 and SK-OV-3 cell lines, licochalocone A induced a decrease in Bid, Bcl-2, Bcl-xL and survivin protein levels; an increase in Bax levels; loss of the mitochondrial transmembrane potential; cytochrome c release; activation of caspases (-8, -9 and -3); cleavage of PARP-1; and an increase in the tumor suppressor p53 levels. YC-1 enhanced licochalcone A-induced apoptosis-related protein activation, nuclear damage and cell death. These results suggest that YC-1 may potentiate the apoptotic effect of licochalcone A on ovarian carcinoma cell lines by increasing the activation of the caspase-8- and Bid-dependent pathway and the mitochondria-mediated apoptotic pathway, leading to caspase activation. The combination of licochalcone A and YC-1 may confer a benefit in the treatment of human epithelial ovarian adenocarcinoma.</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/j.ejphar.2012.03.024</identifier><identifier>PMID: 22465181</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>adenocarcinoma ; animal ovaries ; antineoplastic agents ; Antineoplastic Agents, Phytogenic - pharmacology ; apoptosis ; Apoptosis - drug effects ; Apoptosis Regulatory Proteins - metabolism ; Apoptotic process ; Carcinoma - drug therapy ; Carcinoma - metabolism ; Carcinoma - pathology ; Carcinoma, Ovarian Epithelial ; caspases ; Caspases - chemistry ; Caspases - metabolism ; Cell Line, Tumor ; Cell Nucleus - drug effects ; Chalcones - pharmacology ; cytochrome c ; death ; Drug Interactions ; Enzyme Activation - drug effects ; Epithelial ovarian adenocarcinoma cell lines ; Female ; guanylate cyclase ; Guanylate Cyclase - chemistry ; Humans ; Indazoles - pharmacology ; Licochalcone A ; licorice ; membrane potential ; Neoplasm Proteins - agonists ; Neoplasms, Glandular and Epithelial - drug therapy ; Neoplasms, Glandular and Epithelial - metabolism ; Neoplasms, Glandular and Epithelial - pathology ; ovarian neoplasms ; Ovarian Neoplasms - drug therapy ; Ovarian Neoplasms - metabolism ; Ovarian Neoplasms - pathology ; phenol ; Poly (ADP-Ribose) Polymerase-1 ; Poly(ADP-ribose) Polymerases - metabolism ; Promoting effect ; Proteolysis - drug effects ; Signal Transduction - drug effects ; Tumor Suppressor Protein p53 - metabolism ; YC-1</subject><ispartof>European journal of pharmacology, 2012-05, Vol.683 (1-3), p.54-62</ispartof><rights>2012 Elsevier B.V.</rights><rights>Copyright © 2012 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c386t-4bfbecb9666ce0b9110e857758dc995cd2e07502b2148b61d269208d5b0980103</citedby><cites>FETCH-LOGICAL-c386t-4bfbecb9666ce0b9110e857758dc995cd2e07502b2148b61d269208d5b0980103</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.ejphar.2012.03.024$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22465181$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Chung Soo</creatorcontrib><creatorcontrib>Kwak, Sang Won</creatorcontrib><creatorcontrib>Kim, Yun Jeong</creatorcontrib><creatorcontrib>Lee, Seon Ae</creatorcontrib><creatorcontrib>Park, Eon Sob</creatorcontrib><creatorcontrib>Myung, Soon Chul</creatorcontrib><creatorcontrib>Kim, Wonyong</creatorcontrib><creatorcontrib>Lee, Min Sung</creatorcontrib><creatorcontrib>Lee, Jeong Jae</creatorcontrib><title>Guanylate cyclase activator YC-1 potentiates apoptotic effect of licochalcone A on human epithelial ovarian carcinoma cells via activation of death receptor and mitochondrial pathways</title><title>European journal of pharmacology</title><addtitle>Eur J Pharmacol</addtitle><description>Natural phenol licorice compounds have been shown to induce apoptosis in cancer cells. 3-(5′-Hydroxymethyl-2′-furyl)-1-benzyl indazole (YC-1) may enhance the sensitivity of cancer cells to anticancer drugs. However, the combined effect of licochalcone A and YC-1 on cell death in ovarian cancer cells has not been studied. We assessed the combined effect of licochalcone A and YC-1 on apoptosis in human epithelial ovarian carcinoma cell lines in relation to the cell death process. In the OVCAR-3 and SK-OV-3 cell lines, licochalocone A induced a decrease in Bid, Bcl-2, Bcl-xL and survivin protein levels; an increase in Bax levels; loss of the mitochondrial transmembrane potential; cytochrome c release; activation of caspases (-8, -9 and -3); cleavage of PARP-1; and an increase in the tumor suppressor p53 levels. YC-1 enhanced licochalcone A-induced apoptosis-related protein activation, nuclear damage and cell death. These results suggest that YC-1 may potentiate the apoptotic effect of licochalcone A on ovarian carcinoma cell lines by increasing the activation of the caspase-8- and Bid-dependent pathway and the mitochondria-mediated apoptotic pathway, leading to caspase activation. The combination of licochalcone A and YC-1 may confer a benefit in the treatment of human epithelial ovarian adenocarcinoma.</description><subject>adenocarcinoma</subject><subject>animal ovaries</subject><subject>antineoplastic agents</subject><subject>Antineoplastic Agents, Phytogenic - pharmacology</subject><subject>apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>Apoptotic process</subject><subject>Carcinoma - drug therapy</subject><subject>Carcinoma - metabolism</subject><subject>Carcinoma - pathology</subject><subject>Carcinoma, Ovarian Epithelial</subject><subject>caspases</subject><subject>Caspases - chemistry</subject><subject>Caspases - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Cell Nucleus - drug effects</subject><subject>Chalcones - pharmacology</subject><subject>cytochrome c</subject><subject>death</subject><subject>Drug Interactions</subject><subject>Enzyme Activation - drug effects</subject><subject>Epithelial ovarian adenocarcinoma cell lines</subject><subject>Female</subject><subject>guanylate cyclase</subject><subject>Guanylate Cyclase - chemistry</subject><subject>Humans</subject><subject>Indazoles - pharmacology</subject><subject>Licochalcone A</subject><subject>licorice</subject><subject>membrane potential</subject><subject>Neoplasm Proteins - agonists</subject><subject>Neoplasms, Glandular and Epithelial - drug therapy</subject><subject>Neoplasms, Glandular and Epithelial - metabolism</subject><subject>Neoplasms, Glandular and Epithelial - pathology</subject><subject>ovarian neoplasms</subject><subject>Ovarian Neoplasms - drug therapy</subject><subject>Ovarian Neoplasms - metabolism</subject><subject>Ovarian Neoplasms - pathology</subject><subject>phenol</subject><subject>Poly (ADP-Ribose) Polymerase-1</subject><subject>Poly(ADP-ribose) Polymerases - metabolism</subject><subject>Promoting effect</subject><subject>Proteolysis - drug effects</subject><subject>Signal Transduction - drug effects</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>YC-1</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc2O1DAQhCMEYoeFN0DgI5eEtvPrC9JqBAvSShxgD5ysjtMhHiVxsJ1B82S8Ho6yy5GTpfZX1aWuJHnNIePAq_enjE7LgC4TwEUGeQaieJIceFPLFGouniYHAF6kQkp5lbzw_gQApRTl8-RKiKIqecMPyZ_bFefLiIGYvugRPTHUwZwxWMd-HFPOFhtoDiYSnuFil2CD0Yz6nnRgtmej0VYPOGo7E7thdmbDOuHMaDFhoNHgyOwZnYkjjU6b2U7INI2jZ2eDj9tM1EWzjjAMzJGmZQuAc8cmE6K_nTu3WS3x_zde_MvkWY-jp1cP73Vy_-nj9-Pn9O7r7ZfjzV2q86YKadH2LelWVlWlCVrJOVBT1nXZdFrKUneCoC5BtIIXTVvxTlRSQNOVLcgGOOTXybvdd3H210o-qMn4LT3OZFevYhVQNLksRESLHdXOeu-oV4szE7pLhDauUie1V6a2yhTkKlYWZW8eNqztRN0_0WNHEXi7Az1ahT-d8er-W3QoY58FNOVGfNgJipc4G3LKa0Ozps7EUwbVWfP_DH8B1Wa2YQ</recordid><startdate>20120515</startdate><enddate>20120515</enddate><creator>Lee, Chung Soo</creator><creator>Kwak, Sang Won</creator><creator>Kim, Yun Jeong</creator><creator>Lee, Seon Ae</creator><creator>Park, Eon Sob</creator><creator>Myung, Soon Chul</creator><creator>Kim, Wonyong</creator><creator>Lee, Min Sung</creator><creator>Lee, Jeong Jae</creator><general>Elsevier B.V</general><scope>FBQ</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></search><sort><creationdate>20120515</creationdate><title>Guanylate cyclase activator YC-1 potentiates apoptotic effect of licochalcone A on human epithelial ovarian carcinoma cells via activation of death receptor and mitochondrial pathways</title><author>Lee, Chung Soo ; Kwak, Sang Won ; Kim, Yun Jeong ; Lee, Seon Ae ; Park, Eon Sob ; Myung, Soon Chul ; Kim, Wonyong ; Lee, Min Sung ; Lee, Jeong Jae</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c386t-4bfbecb9666ce0b9110e857758dc995cd2e07502b2148b61d269208d5b0980103</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>adenocarcinoma</topic><topic>animal ovaries</topic><topic>antineoplastic agents</topic><topic>Antineoplastic Agents, Phytogenic - pharmacology</topic><topic>apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>Apoptotic process</topic><topic>Carcinoma - drug therapy</topic><topic>Carcinoma - metabolism</topic><topic>Carcinoma - pathology</topic><topic>Carcinoma, Ovarian Epithelial</topic><topic>caspases</topic><topic>Caspases - chemistry</topic><topic>Caspases - metabolism</topic><topic>Cell Line, Tumor</topic><topic>Cell Nucleus - drug effects</topic><topic>Chalcones - pharmacology</topic><topic>cytochrome c</topic><topic>death</topic><topic>Drug Interactions</topic><topic>Enzyme Activation - drug effects</topic><topic>Epithelial ovarian adenocarcinoma cell lines</topic><topic>Female</topic><topic>guanylate cyclase</topic><topic>Guanylate Cyclase - chemistry</topic><topic>Humans</topic><topic>Indazoles - pharmacology</topic><topic>Licochalcone A</topic><topic>licorice</topic><topic>membrane potential</topic><topic>Neoplasm Proteins - agonists</topic><topic>Neoplasms, Glandular and Epithelial - drug therapy</topic><topic>Neoplasms, Glandular and Epithelial - metabolism</topic><topic>Neoplasms, Glandular and Epithelial - pathology</topic><topic>ovarian neoplasms</topic><topic>Ovarian Neoplasms - drug therapy</topic><topic>Ovarian Neoplasms - metabolism</topic><topic>Ovarian Neoplasms - pathology</topic><topic>phenol</topic><topic>Poly (ADP-Ribose) Polymerase-1</topic><topic>Poly(ADP-ribose) Polymerases - metabolism</topic><topic>Promoting effect</topic><topic>Proteolysis - drug effects</topic><topic>Signal Transduction - drug effects</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>YC-1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Chung Soo</creatorcontrib><creatorcontrib>Kwak, Sang Won</creatorcontrib><creatorcontrib>Kim, Yun Jeong</creatorcontrib><creatorcontrib>Lee, Seon Ae</creatorcontrib><creatorcontrib>Park, Eon Sob</creatorcontrib><creatorcontrib>Myung, Soon Chul</creatorcontrib><creatorcontrib>Kim, Wonyong</creatorcontrib><creatorcontrib>Lee, Min Sung</creatorcontrib><creatorcontrib>Lee, Jeong Jae</creatorcontrib><collection>AGRIS</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><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Chung Soo</au><au>Kwak, Sang Won</au><au>Kim, Yun Jeong</au><au>Lee, Seon Ae</au><au>Park, Eon Sob</au><au>Myung, Soon Chul</au><au>Kim, Wonyong</au><au>Lee, Min Sung</au><au>Lee, Jeong Jae</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Guanylate cyclase activator YC-1 potentiates apoptotic effect of licochalcone A on human epithelial ovarian carcinoma cells via activation of death receptor and mitochondrial pathways</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>2012-05-15</date><risdate>2012</risdate><volume>683</volume><issue>1-3</issue><spage>54</spage><epage>62</epage><pages>54-62</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><abstract>Natural phenol licorice compounds have been shown to induce apoptosis in cancer cells. 3-(5′-Hydroxymethyl-2′-furyl)-1-benzyl indazole (YC-1) may enhance the sensitivity of cancer cells to anticancer drugs. However, the combined effect of licochalcone A and YC-1 on cell death in ovarian cancer cells has not been studied. We assessed the combined effect of licochalcone A and YC-1 on apoptosis in human epithelial ovarian carcinoma cell lines in relation to the cell death process. In the OVCAR-3 and SK-OV-3 cell lines, licochalocone A induced a decrease in Bid, Bcl-2, Bcl-xL and survivin protein levels; an increase in Bax levels; loss of the mitochondrial transmembrane potential; cytochrome c release; activation of caspases (-8, -9 and -3); cleavage of PARP-1; and an increase in the tumor suppressor p53 levels. YC-1 enhanced licochalcone A-induced apoptosis-related protein activation, nuclear damage and cell death. These results suggest that YC-1 may potentiate the apoptotic effect of licochalcone A on ovarian carcinoma cell lines by increasing the activation of the caspase-8- and Bid-dependent pathway and the mitochondria-mediated apoptotic pathway, leading to caspase activation. The combination of licochalcone A and YC-1 may confer a benefit in the treatment of human epithelial ovarian adenocarcinoma.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>22465181</pmid><doi>10.1016/j.ejphar.2012.03.024</doi><tpages>9</tpages></addata></record> |
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| subjects | adenocarcinoma animal ovaries antineoplastic agents Antineoplastic Agents, Phytogenic - pharmacology apoptosis Apoptosis - drug effects Apoptosis Regulatory Proteins - metabolism Apoptotic process Carcinoma - drug therapy Carcinoma - metabolism Carcinoma - pathology Carcinoma, Ovarian Epithelial caspases Caspases - chemistry Caspases - metabolism Cell Line, Tumor Cell Nucleus - drug effects Chalcones - pharmacology cytochrome c death Drug Interactions Enzyme Activation - drug effects Epithelial ovarian adenocarcinoma cell lines Female guanylate cyclase Guanylate Cyclase - chemistry Humans Indazoles - pharmacology Licochalcone A licorice membrane potential Neoplasm Proteins - agonists Neoplasms, Glandular and Epithelial - drug therapy Neoplasms, Glandular and Epithelial - metabolism Neoplasms, Glandular and Epithelial - pathology ovarian neoplasms Ovarian Neoplasms - drug therapy Ovarian Neoplasms - metabolism Ovarian Neoplasms - pathology phenol Poly (ADP-Ribose) Polymerase-1 Poly(ADP-ribose) Polymerases - metabolism Promoting effect Proteolysis - drug effects Signal Transduction - drug effects Tumor Suppressor Protein p53 - metabolism YC-1 |
| title | Guanylate cyclase activator YC-1 potentiates apoptotic effect of licochalcone A on human epithelial ovarian carcinoma cells via activation of death receptor and mitochondrial pathways |
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