Sulforaphane enhances the anticancer activity of taxanes against triple negative breast cancer by killing cancer stem cells
Triple negative breast cancer (TNBC) typically exhibits rapid progression, high mortality and faster relapse rates relative to other breast cancer subtypes. In this report we examine the combination of taxanes (paclitaxel or docetaxel) with a breast cancer stem cell (CSC)-targeting agent sulforaphan...
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| Vydané v: | Cancer letters Ročník 394; s. 52 - 64 |
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| Hlavní autori: | , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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Elsevier B.V
28.05.2017
Elsevier Limited |
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| ISSN: | 0304-3835, 1872-7980 |
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| Abstract | Triple negative breast cancer (TNBC) typically exhibits rapid progression, high mortality and faster relapse rates relative to other breast cancer subtypes. In this report we examine the combination of taxanes (paclitaxel or docetaxel) with a breast cancer stem cell (CSC)-targeting agent sulforaphane for use against TNBC. We demonstrate that paclitaxel or docetaxel treatment induces IL-6 secretion and results in expansion of CSCs in TNBC cell lines. Conversely, sulforaphane is capable of preferentially eliminating CSCs, by inhibiting NF-κB p65 subunit translocation, downregulating p52 and consequent downstream transcriptional activity. Sulforaphane also reverses taxane-induced aldehyde dehydrogenase-positive (ALDH+) cell enrichment, and dramatically reduces the size and number of primary and secondary mammospheres formed. In vivo in an advanced treatment orthotopic mouse xenograft model together with extreme limiting dilution analysis (ELDA), the combination of docetaxel and sulforaphane exhibits a greater reduction in primary tumor volume and significantly reduces secondary tumor formation relative to either treatment alone. These results suggest that treatment of TNBCs with cytotoxic chemotherapy would be greatly benefited by the addition of sulforaphane to prevent expansion of and eliminate breast CSCs.
•Standard taxane-based treatment increases inflammatory cytokine secretion.•Paclitaxel and docetaxel enrich the CSC population.•Anti-CSC compound sulforaphane inhibits NF-κB transcriptional activity.•Sulforaphane reverses taxane-induced CSCs enrichment.•Combination greatly reduces primary tumor volume and secondary tumor formation. |
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| AbstractList | Triple negative breast cancer (TNBC) typically exhibits rapid progression, high mortality and faster relapse rates relative to other breast cancer subtypes. In this report we examine the combination of taxanes (paclitaxel or docetaxel) with a breast cancer stem cell (CSC)-targeting agent sulforaphane for use against TNBC. We demonstrate that paclitaxel or docetaxel treatment induces IL-6 secretion and results in expansion of CSCs in TNBC cell lines. Conversely, sulforaphane is capable of preferentially eliminating CSCs, by inhibiting NF-κB p65 subunit translocation, downregulating p52 and consequent downstream transcriptional activity. Sulforaphane also reverses taxane-induced aldehyde dehydrogenase-positive (ALDH+) cell enrichment, and dramatically reduces the size and number of primary and secondary mammospheres formed. In vivo in an advanced treatment orthotopic mouse xenograft model together with extreme limiting dilution analysis (ELDA), the combination of docetaxel and sulforaphane exhibits a greater reduction in primary tumor volume and significantly reduces secondary tumor formation relative to either treatment alone. These results suggest that treatment of TNBCs with cytotoxic chemotherapy would be greatly benefited by the addition of sulforaphane to prevent expansion of and eliminate breast CSCs. Triple negative breast cancer (TNBC) typically exhibits rapid progression, high mortality and faster relapse rates relative to other breast cancer subtypes. In this report we examine the combination of taxanes (paclitaxel or docetaxel) with a breast cancer stem cell (CSC)-targeting agent sulforaphane for use against TNBC. We demonstrate that paclitaxel or docetaxel treatment induces IL-6 secretion and results in expansion of CSCs in TNBC cell lines. Conversely, sulforaphane is capable of preferentially eliminating CSCs, by inhibiting NF-κB p65 subunit translocation, downregulating p52 and consequent downstream transcriptional activity. Sulforaphane also reverses taxane-induced aldehyde dehydrogenase-positive (ALDH+) cell enrichment, and dramatically reduces the size and number of primary and secondary mammospheres formed. In vivo in an advanced treatment orthotopic mouse xenograft model together with extreme limiting dilution analysis (ELDA), the combination of docetaxel and sulforaphane exhibits a greater reduction in primary tumor volume and significantly reduces secondary tumor formation relative to either treatment alone. These results suggest that treatment of TNBCs with cytotoxic chemotherapy would be greatly benefited by the addition of sulforaphane to prevent expansion of and eliminate breast CSCs. Triple negative breast cancer (TNBC) typically exhibits rapid progression, high mortality and faster relapse rates relative to other breast cancer subtypes. In this report we examine the combination of taxanes (paclitaxel or docetaxel) with a breast cancer stem cell (CSC)-targeting agent sulforaphane for use against TNBC. We demonstrate that paclitaxel or docetaxel treatment induces IL-6 secretion and results in expansion of CSCs in TNBC cell lines. Conversely, sulforaphane is capable of preferentially eliminating CSCs, by inhibiting NF-κB p65 subunit translocation, downregulating p52 and consequent downstream transcriptional activity. Sulforaphane also reverses taxane-induced aldehyde dehydrogenase-positive (ALDH+) cell enrichment, and dramatically reduces the size and number of primary and secondary mammospheres formed. In vivo in an advanced treatment orthotopic mouse xenograft model together with extreme limiting dilution analysis (ELDA), the combination of docetaxel and sulforaphane exhibits a greater reduction in primary tumor volume and significantly reduces secondary tumor formation relative to either treatment alone. These results suggest that treatment of TNBCs with cytotoxic chemotherapy would be greatly benefited by the addition of sulforaphane to prevent expansion of and eliminate breast CSCs. •Standard taxane-based treatment increases inflammatory cytokine secretion.•Paclitaxel and docetaxel enrich the CSC population.•Anti-CSC compound sulforaphane inhibits NF-κB transcriptional activity.•Sulforaphane reverses taxane-induced CSCs enrichment.•Combination greatly reduces primary tumor volume and secondary tumor formation. Triple negative breast cancer (TNBC) typically exhibits rapid progression, high mortality and faster relapse rates relative to other breast cancer subtypes. In this report we examine the combination of taxanes (paclitaxel or docetaxel) with a breast cancer stem cell (CSC)-targeting agent sulforaphane for use against TNBC. We demonstrate that paclitaxel or docetaxel treatment induces IL-6 secretion and results in expansion of CSCs in TNBC cell lines. Conversely, sulforaphane is capable of preferentially eliminating CSCs, by inhibiting NF- Kappa B p65 subunit translocation, downregulating p52 and consequent downstream transcriptional activity. Sulforaphane also reverses taxane-induced aldehyde dehydrogenase-positive (ALDH+) cell enrichment, and dramatically reduces the size and number of primary and secondary mammospheres formed. In vivo in an advanced treatment orthotopic mouse xenograft model together with extreme limiting dilution analysis (ELDA), the combination of docetaxel and sulforaphane exhibits a greater reduction in primary tumor volume and significantly reduces secondary tumor formation relative to either treatment alone. These results suggest that treatment of TNBCs with cytotoxic chemotherapy would be greatly benefited by the addition of sulforaphane to prevent expansion of and eliminate breast CSCs. Abstract Triple negative breast cancer (TNBC) typically exhibits rapid progression, high mortality and faster relapse rates relative to other breast cancer subtypes. In this report we examine the combination of taxanes (paclitaxel or docetaxel) with a breast cancer stem cell (CSC)-targeting agent sulforaphane for use against TNBC. We demonstrate that paclitaxel or docetaxel treatment induces IL-6 secretion and results in expansion of CSCs in TNBC cell lines. Conversely, sulforaphane is capable of preferentially eliminating CSCs, by inhibiting NF-κB p65 subunit translocation, downregulating p52 and consequent downstream transcriptional activity. Sulforaphane also reverses taxane-induced aldehyde dehydrogenase-positive (ALDH+) cell enrichment, and dramatically reduces the size and number of primary and secondary mammospheres formed. In vivo in an advanced treatment orthotopic mouse xenograft model together with extreme limiting dilution analysis (ELDA), the combination of docetaxel and sulforaphane exhibits a greater reduction in primary tumor volume and significantly reduces secondary tumor formation relative to either treatment alone. These results suggest that treatment of TNBCs with cytotoxic chemotherapy would be greatly benefited by the addition of sulforaphane to prevent expansion of and eliminate breast CSCs. Triple negative breast cancer (TNBC) typically exhibits rapid progression, high mortality and faster relapse rates relative to other breast cancer subtypes. In this report we examine the combination of taxanes (paclitaxel or docetaxel) with a breast cancer stem cell (CSC)-targeting agent sulforaphane for use against TNBC. We demonstrate that paclitaxel or docetaxel treatment induces IL-6 secretion and results in expansion of CSCs in TNBC cell lines. Conversely, sulforaphane is capable of preferentially eliminating CSCs, by inhibiting NF-κB p65 subunit translocation, downregulating p52 and consequent downstream transcriptional activity. Sulforaphane also reverses taxane-induced aldehyde dehydrogenase-positive (ALDH+) cell enrichment, and dramatically reduces the size and number of primary and secondary mammospheres formed.In vivoin an advanced treatment orthotopic mouse xenograft model together with extreme limiting dilution analysis (ELDA), the combination of docetaxel and sulforaphane exhibits a greater reduction in primary tumor volume and significantly reduces secondary tumor formation relative to either treatment alone. These results suggest that treatment of TNBCs with cytotoxic chemotherapy would be greatly benefited by the addition of sulforaphane to prevent expansion of and eliminate breast CSCs. |
| Author | McDermott, Sean P. Burnett, Joseph P. Sun, Lichao Wicha, Max S. Paholak, Hayley J. Li, Yanyan Sun, Duxin Shah, Ronak B. Tsume, Yasuhiro Bai, Shuhua Lim, Gi Lim, Rebekah Zhang, Tao |
| AuthorAffiliation | a Department of Pharmaceutical Sciences, College of Pharmacy, University of Michigan, Ann Arbor, MI 48109, USA b School of Science and Humanities, Husson University, Bangor, ME 04401, USA c Department of Basic Pharmaceutical Sciences, School of Pharmacy, Husson University, Bangor, ME 04401, USA d Department of Internal Medicine, Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI 48109, USA |
| AuthorAffiliation_xml | – name: d Department of Internal Medicine, Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI 48109, USA – name: b School of Science and Humanities, Husson University, Bangor, ME 04401, USA – name: c Department of Basic Pharmaceutical Sciences, School of Pharmacy, Husson University, Bangor, ME 04401, USA – name: a Department of Pharmaceutical Sciences, College of Pharmacy, University of Michigan, Ann Arbor, MI 48109, USA |
| Author_xml | – sequence: 1 givenname: Joseph P. surname: Burnett fullname: Burnett, Joseph P. organization: Department of Pharmaceutical Sciences, College of Pharmacy, University of Michigan, Ann Arbor, MI 48109, USA – sequence: 2 givenname: Gi surname: Lim fullname: Lim, Gi organization: School of Science and Humanities, Husson University, Bangor, ME 04401, USA – sequence: 3 givenname: Yanyan surname: Li fullname: Li, Yanyan organization: School of Science and Humanities, Husson University, Bangor, ME 04401, USA – sequence: 4 givenname: Ronak B. surname: Shah fullname: Shah, Ronak B. organization: Department of Pharmaceutical Sciences, College of Pharmacy, University of Michigan, Ann Arbor, MI 48109, USA – sequence: 5 givenname: Rebekah surname: Lim fullname: Lim, Rebekah organization: Department of Basic Pharmaceutical Sciences, School of Pharmacy, Husson University, Bangor, ME 04401, USA – sequence: 6 givenname: Hayley J. surname: Paholak fullname: Paholak, Hayley J. organization: Department of Pharmaceutical Sciences, College of Pharmacy, University of Michigan, Ann Arbor, MI 48109, USA – sequence: 7 givenname: Sean P. surname: McDermott fullname: McDermott, Sean P. organization: Department of Internal Medicine, Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI 48109, USA – sequence: 8 givenname: Lichao surname: Sun fullname: Sun, Lichao organization: Department of Pharmaceutical Sciences, College of Pharmacy, University of Michigan, Ann Arbor, MI 48109, USA – sequence: 9 givenname: Yasuhiro surname: Tsume fullname: Tsume, Yasuhiro organization: Department of Pharmaceutical Sciences, College of Pharmacy, University of Michigan, Ann Arbor, MI 48109, USA – sequence: 10 givenname: Shuhua surname: Bai fullname: Bai, Shuhua organization: Department of Basic Pharmaceutical Sciences, School of Pharmacy, Husson University, Bangor, ME 04401, USA – sequence: 11 givenname: Max S. surname: Wicha fullname: Wicha, Max S. organization: Department of Internal Medicine, Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI 48109, USA – sequence: 12 givenname: Duxin surname: Sun fullname: Sun, Duxin email: duxins@med.umich.edu organization: Department of Pharmaceutical Sciences, College of Pharmacy, University of Michigan, Ann Arbor, MI 48109, USA – sequence: 13 givenname: Tao surname: Zhang fullname: Zhang, Tao email: zhangt@husson.edu organization: Department of Basic Pharmaceutical Sciences, School of Pharmacy, Husson University, Bangor, ME 04401, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28254410$$D View this record in MEDLINE/PubMed |
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| Keywords | IL ELDA Docetaxel Cancer stem cell ALDH CSC PAC Sulforaphane Paclitaxel DOC SFN TNBC Triple negative breast cancer paclitaxel sulforaphane extreme limiting dilution analysis cancer stem cell docetaxel aldehyde dehydrogenase-positive triple negative breast cancer interleukin |
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| PublicationCentury | 2000 |
| PublicationDate | 2017-05-28 |
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| PublicationPlace | Ireland |
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| PublicationTitle | Cancer letters |
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| PublicationYear | 2017 |
| Publisher | Elsevier B.V Elsevier Limited |
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| Title | Sulforaphane enhances the anticancer activity of taxanes against triple negative breast cancer by killing cancer stem cells |
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