PDGF-D/PDGF-ββ Receptor-Regulated Chemotaxis of Malignant Mesothelioma Cells

被引：13

作者：

Okada, Asuka ^{[1
,2
]}

Yaguchi, Takahiro ^{[1
]}

Kanno, Takeshi ^{[1
]}

Gotoh, Akinobu ^{[3
]}

Nakano, Takashi ^{[2
]}

Nishizaki, Tomoyuki ^{[1
]}

机构：

[1] Hyogo Coll Med, Dept Physiol, Div Bioinformat, Nishinomiya, Hyogo 6638501, Japan

[2] Hyogo Coll Med, Dept Thorac Oncol, Nishinomiya, Hyogo 6638501, Japan

[3] Hyogo Coll Med, Inst Adv Med Sci, Lab Cell & Gene Therapy, Nishinomiya, Hyogo 6638501, Japan

来源：

CELLULAR PHYSIOLOGY AND BIOCHEMISTRY | 2012年 / 29卷 / 1-2期

关键词：

Malignant mesothelioma cell; Chemotaxis; PDGF-beta beta receptor; ROCK; ERK; URINARY TRYPSIN-INHIBITOR; GROWTH-FACTOR-D; PLASMINOGEN-ACTIVATOR; PLEURAL MESOTHELIOMA; CARCINOMA-CELLS; CANCER-CELLS; BIOLOGY; OVEREXPRESSION; PROGRESSION; METASTASIS;

D O I：

10.1159/000337605

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Background/Aims: Our earlier study suggested that platelet-derived growth factor (PDGF)-beta beta receptor regulates chemotaxis of human malignant mesothelioma cells such as MSTO-211H, NCIH-2052, NCIH-2452, and NCIH-28 cells, but not non-malignant Met5A cells. The present study was designed to gain further insight into the PDGF-beta beta receptor signals underlying the chemotaxis. Methods: PDGF-D secreted from cells, activation of Akt and ERK, and cell migration were monitored for cells with and without knocking-down PDGF-beta beta receptor. Results: FBS significantly stimulated PDGF-D secretion from malignant mesothelioma cells, but not Met5A cells. PDGF-D activated Akt and ERK in both the nonmalignant and malignant cells. PDGF-D significantly facilitated migration of malignant mesothelioma cells, but not Met5A cells, with the extent varying among the cell types. The facilitatory action of PDGF-D was clearly prevented by knocking-down PDGF-beta beta receptor or inhibitors of PI3 kinase, PDK1, Akt, Rac1, ROCK, and MEK. Conclusion: The results of the present study indicate that PDGF-D promotes malignant mesothelioma cell chemotaxis through PDGF-beta beta receptor signaling pathways along a PI3 kinase/PDK1/Akt/Rac1/ROCK axis and relevant to ERK activation. Copyright (C) 2012 S. Karger AG, Basel

引用

页码：241 / 250

页数：10

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