The role of C1QBP in CSF-1-dependent PKCζ activation and macrophage migration

被引：10

作者：

Wang, Yong ^{[1
]}

Su, Jing ^{[2
]}

Yuan, Bo ^{[2
]}

Fu, Donghe ^{[2
]}

Niu, Yuanjie ^{[1
]}

Yue, Dan ^{[2
]}

机构：

[1] Tianjin Med Univ, Tianjin Inst Urol, Tianjin Med Univ Hosp 2, Dept Urol, Tianjin 300211, Peoples R China

[2] Tianjin Med Univ, Sch Lab Med, Tianjin 300203, Peoples R China

来源：

EXPERIMENTAL CELL RESEARCH | 2018年 / 362卷 / 01期

基金：

中国国家自然科学基金;

关键词：

C1QBP; CSF-1; Migration; Macrophage; PKC zeta; COLONY-STIMULATING FACTOR; RENAL-CELL CARCINOMA; TUMOR-ASSOCIATED MACROPHAGES; BINDING-PROTEIN; GLOBULAR HEADS; INTEGRIN TRAFFICKING; EXPRESSION; RECEPTOR; CANCER; CSF-1;

D O I：

10.1016/j.yexcr.2017.09.038

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Macrophages view as double agents in tumor progression. Trafficking of macrophages to the proximity of tumors is mediated by colony-stimulating factor-1 (CSF-1), a growth factor. In this study, we investigated the role of complement1q-binding protein (C1QBP)/ atypical protein kinase C zeta (PKC zeta) in CSF-1-induced macrophage migration. Disruption of C1QBP expression impaired chemotaxis and adhesion of macrophage. Phosphorylation of PKC zeta is an essential component in macrophage chemotaxis signaling pathway. C1QBP could interact with PKC zeta in macrophage. C1QBP knockdown inhibited CSF-1 induced phosphorylation of PKC zeta and integrin-beta 1. However, C1QBP knockdown didn't affect the phosphorylation of PKC zeta induced by MCP-1. Furthermore, CSF-1 from RCC cell condition medium promoted macrophage chemotaxis and adhesion. Taken together, our results demonstrated that C1QBP plays an essential role in CSF-1 induced migration of macrophages.

引用

页码：11 / 16

页数：6

共 43 条

[21] Macrophages, innate immunity and cancer: balance, tolerance, and diversity
Mantovani, Alberto
Sica, Antonio
[J]. CURRENT OPINION IN IMMUNOLOGY, 2010, 22 (02) : 231 - 237
[22] Linking tumor-associated macrophages, inflammation, and intestinal tumorigenesis: role of MCP-1
McClellan, Jamie L.
Davis, J. Mark
Steiner, Jennifer L.
Enos, Reilly T.
Jung, Seung H.
Carson, James A.
Pena, Maria M.
Carnevale, Kevin A.
Berger, Franklin G.
Murphy, E. Angela
[J]. AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 2012, 303 (10): : G1087 - G1095
[23] Inhibition of the differentiation of dendritic cells from CD34+ progenitors by tumor cells:: Role of interleukin-6 and macrophage colony-stimulating factor
Menetrier-Caux, C
Montmain, G
Dieu, MC
Bain, C
Favrot, MC
Caux, C
Blay, JY
[J]. BLOOD, 1998, 92 (12) : 4778 - 4791
[24] Autocrine CSF-1 and CSF-1 Receptor Coexpression Promotes Renal Cell Carcinoma Growth
Menke, Julia
Kriegsmann, Joerg
Schimanski, Carl Christoph
Schwartz, Melvin M.
Schwarting, Andreas
Kelley, Vicki R.
[J]. CANCER RESEARCH, 2012, 72 (01) : 187 - 200
[25] p32 protein, a splicing factor 2-associated protein, is localized in mitochondrial matrix and is functionally important in maintaining oxidative phosphorylation
Muta, T
Kang, D
Kitajima, S
Fujiwara, T
Hamasaki, N
[J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (39) : 24363 - 24370
[26] Expression of gClq-R/p33 and its major ligands in human atherosclerotic lesions
Peerschke, EIB
Minta, JO
Zhou, SZ
Bini, A
Gotlieb, A
Colman, RW
Ghebrehiwet, B
[J]. MOLECULAR IMMUNOLOGY, 2004, 41 (08) : 759 - 766
[27] Trophic macrophages in development and disease
Pollard, Jeffrey W.
[J]. NATURE REVIEWS IMMUNOLOGY, 2009, 9 (04) : 259 - 270
[28] Roth P, 1992, Curr Top Microbiol Immunol, V181, P141
[29] Receptor for the globular heads of Clq (gClq-R, p33, hyaluronan-binding protein) is preferentially expressed by adenocarcinoma cells
Rubinstein, DB
Stortchevoi, A
Boosalis, M
Ashfaq, R
Ghebrehiwet, B
Peerschke, EIB
Calvo, F
Guillaume, T
[J]. INTERNATIONAL JOURNAL OF CANCER, 2004, 110 (05) : 741 - 750
[30] Shrihari TG, 2017, ECANCERMEDICALSCIENC, V11, DOI 10.3332/ecancer.2017.721

← 1 2 3 4 5 →