Published online before print February 6, 2009
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is required for migration of macrophages
,1
* Tianjin Medical University Cancer Institute and Hospital, Research Center of Basic Medical Sciences, Tianjin, China; and
Tianjin Medical College, Tianjin, China
2 Correspondence: Tianjin Medical University, Research Center of Basic Medical Sciences and Cancer Institute and Hospital, Tianjin, 300060, China. E-mail: zhangning{at}tijmu.edu.cn
ABSTRACT
The crosstalk, mediated by chemoattractants, between cancer cells and tumor-associated macrophages, plays an important role in tumor invasion and metastasis. Our previous study reported that atypical protein kinase C
(PKC
) regulates epidermal growth factor-induced chemotaxis of human breast cancer cells. In this study, we investigated the role of PKC
in CSF-1-induced chemotaxis of macrophages. Knockdown of PKC
by small interference RNA impaired CSF-1-induced chemotaxis of human acute monocytic leukemia cell line THP-1, which was probably a result of a decrease in CSF-1-induced phosphorylation of LIN-11, Is11, and MEC-3 protein domain kinase (LIMK)/cofilin and actin polymerization. Furthermore, silencing PKC
expression also impaired migration of mouse peritoneal macrophages. Scratch analysis indicated that PKC
was required for macrophage migration. Therefore, PKC
is required for CSF-1-induced chemotaxis of macrophages. Blocking activation of PKC
will be a novel strategy to inhibit cancer metastasis by blocking migration of cancer cells and macrophages.
Key Words: CSF-1 chemokine metastasis tumor-associated macrophages
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