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Sulforaphane, a dietary component of broccoli/broccoli sprouts, inhibits breast cancer stem cells

Li Y, Zhang T, Korkaya H, Liu S, Lee HF, Newman B, Yu Y, Clouthier SG, Schwartz SJ, Wicha MS, Sun D

Clinical cancer research : an official journal of the American Association for Cancer Research · 391 citas

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Cómo se estudió

Diseño
Estudio in vitro o de mecanismos (clasificado por nuestro filtro de IA)
Estudiado en
Personas, más trabajo en animales o laboratorio
Resultado principal
Solo mecanismos

Quién lo pagó

Financiación
Financiación independiente
Universidad u hospital
Barbara Ann Karmanos Cancer Institute
Gobierno
National Institutes of Health
Universidad u hospital
School of Medicine, Stanford University
Universidad u hospital
Ludwig Center at Harvard
Gobierno
National Cancer Institute
Gobierno
National Center for Research Resources
Gobierno
NCI NIH HHS
Gobierno
NCRR NIH HHS
Subvenciones
National Cancer Institute (P30CA016058); National Center for Research Resources (UL1 RR025755); National Cancer Institute (R01-CA120023)

Según 8 financiadores declarados.

Publicación

Publicado
2010-04-14 · Clin Cancer Res · vol. 16 · número 9 · págs. 2580–2590
Editorial
American Association for Cancer Research
Citado
569 citas · más que el 100% de estudios similares · 16.5× el promedio de su campo
Impacto
Entre el 10 % más citado de su campo
Referencias
51 trabajos
Acceso
Lectura gratuita
Áreas de investigación
Genomics, phytochemicals, and oxidative stress · Bioactive natural compounds · Curcumin's Biomedical Applications
Palabras clave
Sulforaphane, Cancer stem cell, Wnt signaling pathway, Cancer research, Breast cancer, Population, Aldehyde dehydrogenase, Stem cell, Chemistry, Cancer, Medicine, Pharmacology, Internal medicine, Biology, Biochemistry, Signal transduction, Cell biology, Enzyme
MeSH
cell line, tumor, spheroids, cellular, animals, mice, inbred nod, humans, mice, mice, scid, brassica, breast neoplasms, mammary neoplasms, experimental, thiocyanates, isothiocyanates, sulfoxides, isoenzymes, aldehyde dehydrogenase, anticarcinogenic agents, blotting, western, xenograft model antitumor assays, signal transduction, apoptosis, cell proliferation, dose-response relationship, drug, dietary supplements, female, retinal dehydrogenase, wnt proteins, beta catenin, neoplastic stem cells, seedlings, aldehyde dehydrogenase 1 family

11 autores

  • Yanyan Li🇺🇸University of Michigan; The Ohio State University
  • Tao Zhang🇺🇸University of Michigan; The Ohio State University
  • Hasan Körkaya🇺🇸University of Michigan; The Ohio State University
  • Suling Liu🇺🇸University of Michigan; The Ohio State University
  • Hsiu-Fang Lee🇺🇸University of Michigan; The Ohio State University
  • Bryan W. Newman🇺🇸University of Michigan; The Ohio State University
  • Yanke Yu🇺🇸University of Michigan; The Ohio State University
  • Shawn G. Clouthier🇺🇸University of Michigan; The Ohio State University
  • Steven J. Schwartz🇺🇸 · autor de correspondenciaUniversity of Michigan; The Ohio State University
  • Max S. Wicha🇺🇸 · autor de correspondenciaUniversity of Michigan; The Ohio State University
  • Duxin Sun🇺🇸 · autor de correspondenciaUniversity of Michigan; The Ohio State University

Resumen

El texto original del estudio, en el idioma en que se publicó.

Purpose

The existence of cancer stem cells (CSCs) in breast cancer has profound implications for cancer prevention. In this study, we evaluated sulforaphane, a natural compound derived from broccoli/broccoli sprouts, for its efficacy to inhibit breast CSCs and its potential mechanism.

Experimental design

Aldefluor assay and mammosphere formation assay were used to evaluate the effect of sulforaphane on breast CSCs in vitro. A nonobese diabetic/severe combined immunodeficient xenograft model was used to determine whether sulforaphane could target breast CSCs in vivo, as assessed by Aldefluor assay, and tumor growth upon cell reimplantation in secondary mice. The potential mechanism was investigated using Western blotting analysis and beta-catenin reporter assay.

Results

Sulforaphane (1-5 micromol/L) decreased aldehyde dehydrogenase-positive cell population by 65% to 80% in human breast cancer cells (P 50% in nonobese diabetic/severe combined immunodeficient xenograft tumors (P = 0.003). Sulforaphane eliminated breast CSCs in vivo, thereby abrogating tumor growth after the reimplantation of primary tumor cells into the secondary mice (P < 0.01). Western blotting analysis and beta-catenin reporter assay showed that sulforaphane downregulated the Wnt/beta-catenin self-renewal pathway.

Conclusions

Sulforaphane inhibits breast CSCs and downregulates the Wnt/beta-catenin self-renewal pathway. These findings support the use of sulforaphane for the chemoprevention of breast cancer stem cells and warrant further clinical evaluation.

Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial.

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