Differential Roles of Carboxylated and Uncarboxylated Osteocalcin in Prostate Cancer Growth

Yoshikazu Hayashi^1,2, Tomoyo Kawakubo-Yasukochi^1,4, Akiko Mizokami^1,3, Hiroshi Takeuchi⁵, Seiji Nakamura², Masato Hirata^1✉

1. Laboratory of Molecular and Cellular Biochemistry, Faculty of Dental Science, Kyushu University, Fukuoka 812-8582, Japan
2. Section of Oral and Maxillofacial Oncology, Faculty of Dental Science, Kyushu University, Fukuoka 812-8582, Japan
3. OBT Research Center, Faculty of Dental Science, Kyushu University, Fukuoka 812-8582, Japan
4. Department of Immunological and Molecular Pharmacology, Faculty of Pharmaceutical Science, Fukuoka University, Fukuoka 814-0180, Japan
5. Division of Applied Pharmacology, Kyushu Dental University, Kitakyushu 803-8580, Japan.

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Citation:
Hayashi Y, Kawakubo-Yasukochi T, Mizokami A, Takeuchi H, Nakamura S, Hirata M. Differential Roles of Carboxylated and Uncarboxylated Osteocalcin in Prostate Cancer Growth. J Cancer 2016; 7(12):1605-1609. doi:10.7150/jca.15523. Available from http://www.jcancer.org/v07p1605.htm

Abstract

Serum levels of osteocalcin (OC), a bone matrix non-collagenous protein secreted by osteoblasts, are correlated with pathological bone remodeling such as the bone metastasis of cancer, as well as physiological bone turnover. The pathological roles in prostate cancer growth of the two existing types of serum OC, γ-carboxylated (GlaOC) and lower- (or un-) carboxylated (GluOC), have not yet been discriminatively examined. In the present study, we demonstrate that normal prostate epithelial cell growth was promoted by both types of OC, while growth of cancer cells in the prostate was accelerated by GlaOC but suppressed by GluOC. We suggest that OC regulates prostate cancer growth depending on the γ-carboxylation, in part by triggering reduced phosphorylation of receptor tyrosine kinases.

Keywords: osteocalcin, prostate cancer