Autophagy inhibition enhances sulforaphane-induced apoptosis in human breast cancer cells
Kanematsu S, Uehara N, Miki H, Yoshizawa K, Kawanaka A, Yuri T, Tsubura A
Anticancer research · 119 citas
Etiquetas de revisión
Financiación no declaradaSolo mecanismosDatos neutrales que nuestra revisión registró sobre cómo se hizo este estudio. Describen el método, nunca si nos gusta el resultado.
Cómo se estudió
- Diseño
- Estudio in vitro o de mecanismos (clasificado por nuestro filtro de IA)
- Estudiado en
- Células o muestras de laboratorio
- Resultado principal
- Solo mecanismos
Quién lo pagó
- Financiación
- Financiación no declarada
Publicación
- Publicado
- 2010-09-01 · Anticancer Res · vol. 30 · número 9 · págs. 3381–90
- Editorial
- National Institutes of Health
- Citado
- 147 citas · más que el 96% de estudios similares · 4.5× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 41 trabajos
- Acceso
- De pago
- Áreas de investigación
- Genomics, phytochemicals, and oxidative stress · Curcumin's Biomedical Applications · Autophagy in Disease and Therapy
- Palabras clave
- Autophagy, Apoptosis, Viability assay, Programmed cell death, Cell cycle, Trypan blue, Cancer cell, Biology, Flow cytometry, Cyclin B1, Molecular biology, Cell growth, MTT assay, Cancer research, Cell biology, Chemistry, Cyclin-dependent kinase 1, Cancer, Biochemistry
- MeSH
- cell line, tumor, humans, breast neoplasms, thiocyanates, isothiocyanates, sulfoxides, anticarcinogenic agents, enzyme inhibitors, microscopy, electron, transmission, fluorescent antibody technique, blotting, western, flow cytometry, cell separation, signal transduction, apoptosis, cell proliferation, autophagy, female
7 autores
- Sayaka Kanematsu🇯🇵Kansai Medical University
- Norihisa Uehara🇯🇵Kansai Medical University
- Hisanori Miki🇯🇵Kansai Medical University
- Katsuhiko Yoshizawa🇯🇵Kansai Medical University
- Ayako Kawanaka🇯🇵Kansai Medical University
- Takashi Yuri🇯🇵Kansai Medical University
- Airo Tsubura🇯🇵Kansai Medical University
Resumen
El texto original del estudio, en el idioma en que se publicó.
Aim
Sulforaphane (SFN), which is present in cruciferous vegetables, induces growth arrest and/or cell death in cancer of various organs. The involvement of autophagy in the SFN-induced apoptotic death of human breast cancer cells was investigated.
Materials and methods
Cell proliferation and viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and trypan blue exclusion assay. Flow cytometry, immunofluorescence, electron microscopy, and Western blot analysis were used for detection of apoptosis and autophagy, and the role of autophagy was assessed using autophagy inhibitors.
Results
SFN dose- and time-dependently retarded the growth and induced cell death in MCF-7 and MDA-MB-231 human breast cancer cells. In MDA-MB-231 cells, 30 μM SFN caused S and G2/M cell-cycle arrest associated with increased p21WAF1 and p27KIP1 levels and decreased cyclin A, cyclin B1 and CDC2 levels. Cell death was due to apoptosis with increased caspase-3 and lowered BCL-2 levels. In addition, the SFN-treated cells exhibited autophagy, as characterized by the appearance of autophagic vacuoles by electron microscopy, the accumulation of acidic vesicular organelles by flow cytometry, and the punctuate patterns of microtubule-associated protein 1 light chain 3 (LC3) by fluorescein microscopy. The levels of LC3-I and -II proteins (processed forms of LC3-I) and LC3 mRNA were increased. Treatment with autophagy inhibitor bafilomycin A1 (but not 3-methyladenine) with SFN significantly enhanced apoptosis, which was accompanied by increases in the level of BAX and the cleavage of caspase-3 and poly(ADP-ribose)polymerase (PARP)-1 and decreases in the mitochondrial membrane potential (ΔΨm).
Conclusion
These results indicate a cytoprotective role of autophagy against SFN-induced apoptosis and that the combination of SFN treatment with autophagy inhibition may be a promising strategy for breast cancer control.
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