IGF-I and MAP kinase involvement in the stimulatory effects of LNCaP prostate cancer cell conditioned media on cell proliferation and protein synthesis in MC3T3-E1 osteoblastic cells
IGF-I and MAP kinase involvement in the stimulatory effects of LNCaP prostate cancer cell conditioned media on cell proliferation and protein synthesis in MC3T3-E1 osteoblastic cells
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DOI：
10.1002/jcb.10726
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发表时间：
2003-12-01
影响因子：
4
通讯作者：
Stern, PH
中科院分区：
文献类型：
--
作者：
Bhattacharyya, RS;Stern, PH
前列腺癌的骨转移导致异常的新骨形成，然而，所涉及的因素和导致反应的途径并不完全确定。我们研究了LNCaP前列腺癌细胞条件培养基（CM）对成骨细胞刺激作用的机制。将MC 3 T3-E1成骨细胞与来自汇合的LNCaP细胞的CM一起培养。LNCaP CM刺激MC 3 T3-E1细胞的MAP激酶、细胞增殖（3 H-胸苷掺入）和蛋白质合成（C-14-脯氨酸掺入）。细胞增殖和蛋白质合成的增加通过抑制MAP激酶途径来阻止。IGF-I可模拟CM对MC 3 T3-E1细胞的作用，抑制IGF-I的作用可降低LNCaP CM对3 H-胸苷和C-14-脯氨酸掺入的刺激作用和MAP激酶活性。研究结果表明，IGF-I是LNCaP细胞CM对成骨细胞中细胞增殖和蛋白质合成的刺激作用的重要因素，并且MAP激酶是这些作用的信号通路的组成部分。(C)2003 Wiley-Liss，Inc.
Bone metastases from Prostate cancer cause abnormal new bone formation, however, the factors involved and the pathways leading to the response are incompletely defined. We investigated the mechanisms of osteoblast stimulatory effects of LNCaP prostate carcinoma cell conditioned media (CM). MC3T3-E1 osteoblastic cells were cultured with CM from confluent LNCaP cells. LNCaP CM stimulated MAP kinase, cell proliferation (3 H-thymidine incorporation), and protein synthesis (C-14-proline incorporation) in the MC3T3-E1 cells. The increases in cell proliferation and protein synthesis were prevented by inhibition of the MAP kinase pathway. IGF-I mimicked the effects of the CM on the MC3T3-E1 cells and inhibition of IGF-I action decreased the LNCaP CM stimulation of 3 H-thymidine and C-14-proline incorporation and MAP kinase activity. The findings indicate that IGF-I is an important factor for the stimulatory effects of LNCaP cell CM on cell proliferation and protein synthesis in osteoblastic cells, and that MAP kinase is a component of the signaling pathway for these effects. (C) 2003 Wiley-Liss, Inc.