TY - JOUR
T1 - Differential roles of carboxylated and uncarboxylated osteocalcin in prostate cancer growth
AU - Hayashi, Yoshikazu
AU - Kawakubo-Yasukochi, Tomoyo
AU - Mizokami, Akiko
AU - Takeuchi, Hiroshi
AU - Nakamura, Seiji
AU - Hirata, Masato
N1 - Funding Information:
This work was supported by the Japan Society for the Promotion of Science (KAKENHI grants 24229009 to M. H., 26861554 and 16K11496 to T. K-Y., and 26861553 and 16K20421 to A. M. ).
Publisher Copyright:
© Ivyspring International Publisher.
PY - 2016
Y1 - 2016
N2 - 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.
AB - 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.
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U2 - 10.7150/jca.15523
DO - 10.7150/jca.15523
M3 - Article
AN - SCOPUS:85008451502
SN - 1837-9664
VL - 7
SP - 1605
EP - 1609
JO - Journal of Cancer
JF - Journal of Cancer
IS - 12
ER -
