The effectiveness of cucurbitacin B in BRCA1 defective breast cancer cells
Cucurbitacin B (CuB) is one of the potential agents for long term anticancer chemoprevention. Cumulative evidences has shown that cucurbitacin B provides potent cellular biological activities such as hepatoprotective, anti-inflammatory and antimicrobial effects, but the precise mechanism of this age...
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| creator | Promkan, Moltira Dakeng, Sumana Chakrabarty, Subhas Bögler, Oliver Patmasiriwat, Pimpicha |
| description | Cucurbitacin B (CuB) is one of the potential agents for long term anticancer chemoprevention. Cumulative evidences has shown that cucurbitacin B provides potent cellular biological activities such as hepatoprotective, anti-inflammatory and antimicrobial effects, but the precise mechanism of this agent is not clearly understood. We examine the biological effects on cancer cells of cucurbitacin B extracted from a Thai herb, Trichosanthes cucumerina L. The wild type (wt) BRCA1, mutant BRCA1, BRCA1 knocked-down and BRCA1 overexpressed breast cancer cells were treated with the cucurbitacin B and determined for the inhibitory effects on the cell proliferation, migration, invasion, anchorage-independent growth. The gene expressions in the treated cells were analyzed for p21/(Waf1), p27(Kip1) and survivin. Our previous study revealed that loss of BRCA1 expression leads to an increase in survivin expression, which is responsible for a reduction in sensitivity to paclitaxel. In this work, we showed that cucurbitacin B obviously inhibited knocked-down and mutant BRCA1 breast cancer cells rather than the wild type BRCA1 breast cancer cells in regards to the cellular proliferation, migration, invasion and anchorage-independent growth. Furthermore, forcing the cells to overexpress wild type BRCA1 significantly reduced effectiveness of cucurbitacin B on growth inhibition of the endogenous mutant BRCA1 cells. Interestingly, cucurbitacin B promotes the expression of p21/(Waf1) and p27(Kip1) but inhibit the expression of survivin. We suggest that survivin could be an important target of cucurbitacin B in BRCA1 defective breast cancer cells. |
| doi_str_mv | 10.1371/journal.pone.0055732 |
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Cumulative evidences has shown that cucurbitacin B provides potent cellular biological activities such as hepatoprotective, anti-inflammatory and antimicrobial effects, but the precise mechanism of this agent is not clearly understood. We examine the biological effects on cancer cells of cucurbitacin B extracted from a Thai herb, Trichosanthes cucumerina L. The wild type (wt) BRCA1, mutant BRCA1, BRCA1 knocked-down and BRCA1 overexpressed breast cancer cells were treated with the cucurbitacin B and determined for the inhibitory effects on the cell proliferation, migration, invasion, anchorage-independent growth. The gene expressions in the treated cells were analyzed for p21/(Waf1), p27(Kip1) and survivin. Our previous study revealed that loss of BRCA1 expression leads to an increase in survivin expression, which is responsible for a reduction in sensitivity to paclitaxel. In this work, we showed that cucurbitacin B obviously inhibited knocked-down and mutant BRCA1 breast cancer cells rather than the wild type BRCA1 breast cancer cells in regards to the cellular proliferation, migration, invasion and anchorage-independent growth. Furthermore, forcing the cells to overexpress wild type BRCA1 significantly reduced effectiveness of cucurbitacin B on growth inhibition of the endogenous mutant BRCA1 cells. Interestingly, cucurbitacin B promotes the expression of p21/(Waf1) and p27(Kip1) but inhibit the expression of survivin. We suggest that survivin could be an important target of cucurbitacin B in BRCA1 defective breast cancer cells.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0055732</identifier><identifier>PMID: 23393598</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Analysis ; Anticancer properties ; Apoptosis ; Biological effects ; Biology ; Blotting, Western ; BRCA1 protein ; BRCA1 Protein - metabolism ; Breast cancer ; Breast Neoplasms - metabolism ; Cancer ; Cancer cells ; Cancer genetics ; Cancer prevention ; Cancer treatment ; Cell Line, Tumor ; Cell migration ; Cell Movement - drug effects ; Cell Movement - genetics ; Cell proliferation ; Cell Survival - drug effects ; Cell Survival - genetics ; Chemotherapy ; Cucurbitaceae ; Cyclin-dependent kinase inhibitor p21 ; Cyclin-dependent kinase inhibitor p27 ; Defects ; Estrogens ; Gene expression ; Genes ; Humans ; Inflammation ; Lymphocytes B ; Medicine ; Mutation ; Ovarian cancer ; Paclitaxel ; Survivin ; Triterpenes - pharmacology</subject><ispartof>PloS one, 2013-02, Vol.8 (2), p.e55732-e55732</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013. This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-b338474cf6e36b8e0050a43411cc8dc24a8054dc054291ff76b912c2213a59513</citedby><cites>FETCH-LOGICAL-c758t-b338474cf6e36b8e0050a43411cc8dc24a8054dc054291ff76b912c2213a59513</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/PMC3564916/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3564916/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23393598$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Promkan, Moltira</creatorcontrib><creatorcontrib>Dakeng, Sumana</creatorcontrib><creatorcontrib>Chakrabarty, Subhas</creatorcontrib><creatorcontrib>Bögler, Oliver</creatorcontrib><creatorcontrib>Patmasiriwat, Pimpicha</creatorcontrib><title>The effectiveness of cucurbitacin B in BRCA1 defective breast cancer cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Cucurbitacin B (CuB) is one of the potential agents for long term anticancer chemoprevention. Cumulative evidences has shown that cucurbitacin B provides potent cellular biological activities such as hepatoprotective, anti-inflammatory and antimicrobial effects, but the precise mechanism of this agent is not clearly understood. We examine the biological effects on cancer cells of cucurbitacin B extracted from a Thai herb, Trichosanthes cucumerina L. The wild type (wt) BRCA1, mutant BRCA1, BRCA1 knocked-down and BRCA1 overexpressed breast cancer cells were treated with the cucurbitacin B and determined for the inhibitory effects on the cell proliferation, migration, invasion, anchorage-independent growth. The gene expressions in the treated cells were analyzed for p21/(Waf1), p27(Kip1) and survivin. Our previous study revealed that loss of BRCA1 expression leads to an increase in survivin expression, which is responsible for a reduction in sensitivity to paclitaxel. In this work, we showed that cucurbitacin B obviously inhibited knocked-down and mutant BRCA1 breast cancer cells rather than the wild type BRCA1 breast cancer cells in regards to the cellular proliferation, migration, invasion and anchorage-independent growth. Furthermore, forcing the cells to overexpress wild type BRCA1 significantly reduced effectiveness of cucurbitacin B on growth inhibition of the endogenous mutant BRCA1 cells. Interestingly, cucurbitacin B promotes the expression of p21/(Waf1) and p27(Kip1) but inhibit the expression of survivin. We suggest that survivin could be an important target of cucurbitacin B in BRCA1 defective breast cancer cells.</description><subject>Analysis</subject><subject>Anticancer properties</subject><subject>Apoptosis</subject><subject>Biological effects</subject><subject>Biology</subject><subject>Blotting, Western</subject><subject>BRCA1 protein</subject><subject>BRCA1 Protein - metabolism</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - metabolism</subject><subject>Cancer</subject><subject>Cancer cells</subject><subject>Cancer genetics</subject><subject>Cancer prevention</subject><subject>Cancer treatment</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement - drug effects</subject><subject>Cell Movement - genetics</subject><subject>Cell proliferation</subject><subject>Cell Survival - drug effects</subject><subject>Cell Survival - genetics</subject><subject>Chemotherapy</subject><subject>Cucurbitaceae</subject><subject>Cyclin-dependent kinase inhibitor p21</subject><subject>Cyclin-dependent kinase inhibitor p27</subject><subject>Defects</subject><subject>Estrogens</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Lymphocytes B</subject><subject>Medicine</subject><subject>Mutation</subject><subject>Ovarian cancer</subject><subject>Paclitaxel</subject><subject>Survivin</subject><subject>Triterpenes - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Promkan, Moltira</au><au>Dakeng, Sumana</au><au>Chakrabarty, Subhas</au><au>Bögler, Oliver</au><au>Patmasiriwat, Pimpicha</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The effectiveness of cucurbitacin B in BRCA1 defective breast cancer cells</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-02-05</date><risdate>2013</risdate><volume>8</volume><issue>2</issue><spage>e55732</spage><epage>e55732</epage><pages>e55732-e55732</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Cucurbitacin B (CuB) is one of the potential agents for long term anticancer chemoprevention. Cumulative evidences has shown that cucurbitacin B provides potent cellular biological activities such as hepatoprotective, anti-inflammatory and antimicrobial effects, but the precise mechanism of this agent is not clearly understood. We examine the biological effects on cancer cells of cucurbitacin B extracted from a Thai herb, Trichosanthes cucumerina L. The wild type (wt) BRCA1, mutant BRCA1, BRCA1 knocked-down and BRCA1 overexpressed breast cancer cells were treated with the cucurbitacin B and determined for the inhibitory effects on the cell proliferation, migration, invasion, anchorage-independent growth. The gene expressions in the treated cells were analyzed for p21/(Waf1), p27(Kip1) and survivin. Our previous study revealed that loss of BRCA1 expression leads to an increase in survivin expression, which is responsible for a reduction in sensitivity to paclitaxel. In this work, we showed that cucurbitacin B obviously inhibited knocked-down and mutant BRCA1 breast cancer cells rather than the wild type BRCA1 breast cancer cells in regards to the cellular proliferation, migration, invasion and anchorage-independent growth. Furthermore, forcing the cells to overexpress wild type BRCA1 significantly reduced effectiveness of cucurbitacin B on growth inhibition of the endogenous mutant BRCA1 cells. Interestingly, cucurbitacin B promotes the expression of p21/(Waf1) and p27(Kip1) but inhibit the expression of survivin. We suggest that survivin could be an important target of cucurbitacin B in BRCA1 defective breast cancer cells.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23393598</pmid><doi>10.1371/journal.pone.0055732</doi><tpages>e55732</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis Anticancer properties Apoptosis Biological effects Biology Blotting, Western BRCA1 protein BRCA1 Protein - metabolism Breast cancer Breast Neoplasms - metabolism Cancer Cancer cells Cancer genetics Cancer prevention Cancer treatment Cell Line, Tumor Cell migration Cell Movement - drug effects Cell Movement - genetics Cell proliferation Cell Survival - drug effects Cell Survival - genetics Chemotherapy Cucurbitaceae Cyclin-dependent kinase inhibitor p21 Cyclin-dependent kinase inhibitor p27 Defects Estrogens Gene expression Genes Humans Inflammation Lymphocytes B Medicine Mutation Ovarian cancer Paclitaxel Survivin Triterpenes - pharmacology |
| title | The effectiveness of cucurbitacin B in BRCA1 defective breast cancer cells |
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