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Capsaicin causes cell-cycle arrest and apoptosis in ER-positive and -negative breast cancer cells by modulating the EGFR/HER-2 pathway
Oncogene, 10/29/09
Thoennissen NH et al. – The data indicate that capsaicin is a novel modulator of the EGFR/HER–2 pathway in both ER–positive and –negative breast cancer cells with a potential role in the treatment and prevention of human breast cancer.
NH Thoennissen, 10/29/09
| At present, breast cancer is the second leading cause of cancer death in women in the western world, exceeded only by lung cancer. Although significant advances have been made in the treatment, only less than half of the patients treated for localized breast cancer benefit from adjuvant chemotherapy; and most patients with metastatic cancer eventually develop disease that is resistant to therapy. Additionally, systemic treatment of breast cancer may cause acute and chronic toxicities including congestive heart failure, neuropathy, sterility and osteoporosis. In this study, we provide strong evidence that capsaicin, a natural occuring vanilloid receptor agonist, has a profound in vitro as well as in vivo antiproliferative effects against ER-postive and -negative human breast cancer cells. Moreover, the compound markedly inhibited pre-neoplastic mammary gland lesions in a murine organ culture model without any signs for toxicity. Overall, the ability of capsaicin to suppress EGFR, proto-oncogene HER-2 and activated ERK provides a sound basis for further exploring the use of capsaicin either alone or in combination with other agents to prevent recurrence or to reduce growth of breast cancer in patients. |
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