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¹ Department of Pathology, Wakayama Medical University, Kimiidera 811-1, Wakayama 641-0012, Japan² Department of Rehabilitation, Osaka Kawasaki Rehabilitation University, Mizuma 158, Kaizuka City, Osaka 597-0104, Japan³ Department of Advanced Medical Science, Institute of Medical Science, University of Tokyo, Shirokanedai, 4-6-1, Minato-ku, Tokyo 108-8639, Japan

(Correspondence should be addressed to M Nakamura; Email: nakamuram{at}kawasakigakuen.ac.jp)

The mitogen-activated protein kinases (MAPKs) signaling pathway is a potential target in cancer therapy. Constitutive phosphorylated extracellular signal-regulated kinase (ERK1/2), which is one of the MAPKs has been detected in a variety of tumors. Calcitonin (CT) is a polypeptide hormone secreted by the thyroid gland and has been used to treat the osteoporosis and humoral hypercalcemia of malignancy. We report that CT decreases ERK1/2 phosphorylation in cancer cells showing constitutive phosphorylated ERK1/2. In MDA-MB-231 cells, a breast cancer cell line showing constitutive phosphorylated ERK1/2, CT phosphorylated c-Raf at Ser²⁵⁹ via the protein kinase A pathway, resulting in suppression of ERK1/2 phosphorylation. CT significantly reduced the tumor volume of MDA-MB-231 cells showing constitutive phosphorylated ERK1/2 compared with saline buffer. However, CT did not exert any significant effects on the proliferation of MCF-7 cells, a breast cancer cell line, showing non-constitutive phosphorylated ERK1/2. These novel findings indicate that CT may be used to target ERK in the treatment of cancer.

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