Sulforaphane potentiates anticancer effects of doxorubicin and attenuates its cardiotoxicity in a breast cancer model
Bose C, Awasthi S, Sharma R, Beneš H, Hauer-Jensen M, Boerma M, Singh SP
PloS one · 68 citas
Cómo se estudió
- Diseño
- Estudio en animales (clasificado por nuestro filtro de IA)
- Estudiado en
- Personas, más trabajo en animales o laboratorio
- Resultado principal
- Eventos clínicos como enfermedad o muerte
Quién lo pagó
- Financiación
- Financiación independiente
- Organización sin fines de lucro
- American Heart Association
- Gobierno
- National Institutes of Health
- Gobierno
- National Institute on Aging
- Gobierno
- National Institute of General Medical Sciences
- Gobierno
- NIH HHS
- Gobierno
- NIA NIH HHS
- Gobierno
- NIGMS NIH HHS
- Subvenciones
- American Heart Association (14GRNT18890084); National Institute on Aging (R01AG032643); National Institute of General Medical Sciences (P20‐GM109005); National Institutes of Health (14GRNT18890084); American Heart Association (R01 AG032643); National Institute of General Medical Sciences (GM109005); National Institutes of Health (P20GM109005); National Institutes of Health (AG-032643); National Institutes of Health (GM109005); National Institutes of Health (R01 AG032643)
Según 7 financiadores declarados y la declaración de financiación del texto completo.
Publicación
- Publicado
- 2018-03-08 · PLoS One · vol. 13 · número 3 · pág. e0193918
- Editorial
- Public Library of Science
- Citado
- 87 citas · más que el 94% de estudios similares · 3.6× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 88 trabajos
- Acceso
- Acceso abierto (revista) · CC-BY
- Áreas de investigación
- Genomics, phytochemicals, and oxidative stress · Chemotherapy-induced cardiotoxicity and mitigation · Synthesis and Biological Evaluation
- Palabras clave
- Sulforaphane, Cardiotoxicity, Doxorubicin, Breast cancer, Cancer, Medicine, Pharmacology, Cancer research, Oxidative stress, Cancer cell, Toxicity, Internal medicine, Chemotherapy
- MeSH
- cell line, tumor, mitochondria, heart, myocytes, cardiac, animals, humans, rats, rats, sprague-dawley, breast neoplasms, mammary neoplasms, experimental, isothiocyanates, sulfoxides, doxorubicin, anticarcinogenic agents, antineoplastic combined chemotherapy protocols, cytokines, xenograft model antitumor assays, oxidation-reduction, lipid peroxidation, oxidative phosphorylation, oxidative stress, drug synergism, female, nf-e2-related factor 2, cardiotoxicity
7 autores
- Chhanda Bose🇺🇸University of Arkansas for Medical Sciences
- Sanjay Awasthi🇺🇸Texas Tech University Health Sciences Center
- Rajendra Sharma🇺🇸University of Arkansas for Medical Sciences
- Helen Beneš🇺🇸University of Arkansas for Medical Sciences
- Martin Hauer‐Jensen🇺🇸University of Arkansas for Medical Sciences
- Marjan Boerma🇺🇸University of Arkansas for Medical Sciences
- Sharda Prakash Singh🇺🇸 · autor de correspondenciaCentral Arkansas Veterans Healthcare System; University of Arkansas for Medical Sciences; Texas Tech University Health Sciences Center
Resumen
El texto original del estudio, en el idioma en que se publicó.
Breast cancer is the most common malignancy in women of the Western world. Doxorubicin (DOX) continues to be used extensively to treat early-stage or node-positive breast cancer, human epidermal growth factor receptor-2 (HER2)-positive breast cancer, and metastatic disease. We have previously demonstrated in a mouse model that sulforaphane (SFN), an isothiocyanate isolated from cruciferous vegetables, protects the heart from DOX-induced toxicity and damage. However, the effects of SFN on the chemotherapeutic efficacy of DOX in breast cancer are not known. Present studies were designed to investigate whether SFN alters the effects of DOX on breast cancer regression while also acting as a cardioprotective agent. Studies on rat neonatal cardiomyocytes and multiple rat and human breast cancer cell lines revealed that SFN protects cardiac cells but not cancer cells from DOX toxicity. Results of studies in a rat orthotopic breast cancer model indicated that SFN enhanced the efficacy of DOX in regression of tumor growth, and that the DOX dosage required to treat the tumor could be reduced when SFN was administered concomitantly. Additionally, SFN enhanced mitochondrial respiration in the hearts of DOX-treated rats and reduced cardiac oxidative stress caused by DOX, as evidenced by the inhibition of lipid peroxidation, the activation of NF-E2-related factor 2 (Nrf2) and associated antioxidant enzymes. These studies indicate that SFN not only acts synergistically with DOX in cancer regression, but also protects the heart from DOX toxicity through Nrf2 activation and protection of mitochondrial integrity and functions.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY).
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