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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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Autores principales: Promkan, Moltira, Dakeng, Sumana, Chakrabarty, Subhas, Bögler, Oliver, Patmasiriwat, Pimpicha
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3564916/
https://www.ncbi.nlm.nih.gov/pubmed/23393598
http://dx.doi.org/10.1371/journal.pone.0055732
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author Promkan, Moltira
Dakeng, Sumana
Chakrabarty, Subhas
Bögler, Oliver
Patmasiriwat, Pimpicha
author_facet Promkan, Moltira
Dakeng, Sumana
Chakrabarty, Subhas
Bögler, Oliver
Patmasiriwat, Pimpicha
author_sort Promkan, Moltira
collection PubMed
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.
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spelling pubmed-35649162013-02-07 The Effectiveness of Cucurbitacin B in BRCA1 Defective Breast Cancer Cells Promkan, Moltira Dakeng, Sumana Chakrabarty, Subhas Bögler, Oliver Patmasiriwat, Pimpicha PLoS One Research Article 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. Public Library of Science 2013-02-05 /pmc/articles/PMC3564916/ /pubmed/23393598 http://dx.doi.org/10.1371/journal.pone.0055732 Text en https://creativecommons.org/publicdomain/zero/1.0/ This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.
spellingShingle Research Article
Promkan, Moltira
Dakeng, Sumana
Chakrabarty, Subhas
Bögler, Oliver
Patmasiriwat, Pimpicha
The Effectiveness of Cucurbitacin B in BRCA1 Defective Breast Cancer Cells
title The Effectiveness of Cucurbitacin B in BRCA1 Defective Breast Cancer Cells
title_full The Effectiveness of Cucurbitacin B in BRCA1 Defective Breast Cancer Cells
title_fullStr The Effectiveness of Cucurbitacin B in BRCA1 Defective Breast Cancer Cells
title_full_unstemmed The Effectiveness of Cucurbitacin B in BRCA1 Defective Breast Cancer Cells
title_short The Effectiveness of Cucurbitacin B in BRCA1 Defective Breast Cancer Cells
title_sort effectiveness of cucurbitacin b in brca1 defective breast cancer cells
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3564916/
https://www.ncbi.nlm.nih.gov/pubmed/23393598
http://dx.doi.org/10.1371/journal.pone.0055732
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