Stimulation of Motility of Human Renal Cell Carcinoma by SPARC/Osteonectin/BM-40 Associated with Type IV Collagen

Kato, Yukio; Sakai, Naoki; M, Baba; Kaneko, Shotaro; Kondo, Keiichi; Kubota, Yoshinobu; Yao, Masahiro; Shuin, Taro; Saito, Shigeru; Koshika, Shinri; Kawase, Toshio; Miyagi, Yohei; Aoki, Ichiro; Nagashima, Yoji

doi:10.1159/000024503

Cited by 18 publications

(12 citation statements)

References 29 publications

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“…SPARC also induced cell motility of renal cell carcinoma associated with type IV collagen. 16 In addition, SPARC production was well correlated with metastatic ability of mouse B16 melanoma cells in this study. Taken together, SPARC action might be a most effective in tumor intravasation or extravasation in the tumor metastasis process.…”

Section: Resultssupporting

confidence: 64%

“…For example, SPARC is co-expressed with stromelysin-3 in colorectal cancer, 5 and induces production of collagenase, stromelysin and gelatinase B, 13,14 and mediates pro-gelatinase A activation via membrane type 1-MMP (MT1-MMP). 15 In addition, it stimulates migration of human renal cell carcinoma 16 and prostatic cancer. 17 Thus, SPARC is thought to play a role of tumorigenesis and tumor progression.…”

Section: Sparc (Secreted Protein Acidic and Rich In Cysteine)/osteonmentioning

confidence: 99%

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High production of SPARC/osteonectin/BM-40 in mouse metastatic B16 melanoma cell lines

Kato

Frankenne

Noel

et al. 2000

Pathol. Oncol. Res.

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Production of SPARC/osteonectin/BM-40 was determined in mouse B16 melanoma clones BL6 and F10 (high metastatic) and F1 (low metastatic). SPARC was produced greater amount in BL6 and F10 than in F1 cells, showing a good agreement with their metastatic potentials. Moreover, SPARC production was not influenced by culture pH, even in the acidic conditions (≈pH 5.9). Although tumor tissues show often low pH due to excessive amount of acidic metabolites such as lactate, most studies have been done in neutral pH. High SPARC production in the acidic medium, therefore, is thought to be an important potential for tumor invasive behaviour.

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Section: Resultssupporting

confidence: 64%

Section: Sparc (Secreted Protein Acidic and Rich In Cysteine)/osteonmentioning

confidence: 99%

High production of SPARC/osteonectin/BM-40 in mouse metastatic B16 melanoma cell lines

Kato

Frankenne

Noel

et al. 2000

Pathol. Oncol. Res.

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“…Exogenous osteonectin is a chemotactic factor that increases cell migration and invasion of renal (40), prostate, and breast (20) carcinoma cells. In addition, endogenous expression of osteonectin alters the migration of glioma cell lines, with either increased or decreased migration observed depending on the type of extracellular matrix proteins present (41).…”

Section: Resultsmentioning

confidence: 99%

Endogenous Osteonectin/SPARC/BM-40 Expression Inhibits MDA-MB-231 Breast Cancer Cell Metastasis

Koblinski¹,

Kaplan-Singer²,

VanOsdol³

et al. 2005

Cancer Research

107

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Skeletal metastases occur with high incidence in patients with breast cancer and cause long-term skeletal morbidity. Osteonectin (SPARC, BM-40) is a bone matrix factor that is an in vitro chemoattractant for breast and prostate cancer cells. Increased expression of osteonectin is found in malignant breast tumors. We infected MDA-231 breast cancer cells with an adenovirus expressing osteonectin to examine the role of osteonectin expression in breast cancer cells and its effect on metastasis, in particular to bone. Expression of osteonectin did not affect MDA-231 cell proliferation, apoptosis, migration, cell aggregation, or protease cleavage of collagen IV. However, in vitro invasion of these osteonectininfected cells through Matrigel and colony formation on Matrigel was decreased. Interestingly, high osteonectin expression in MDA-231 cells inhibited metastasis in a dosedependent manner to many different organs including bone. The reduction in metastasis may be due to decreased platelettumor cell aggregation, because exogenous osteonectin inhibited platelet aggregation in vitro and the high osteonectin expression in MDA-231 cells reduced tumor cell-induced thrombocytopenia in vivo compared with control-infected cells. These studies suggest that high endogenous expression of osteonectin in breast cancer cells may reduce metastasis via reduced invasive activity and reduced tumor cell-platelet aggregation. (Cancer Res 2005; 65(16): 7370-7)

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“…Transwell chemotactic chamber assay was used for estimation of migration activity of HUVECs according to our previous reports [12,17] with some modifications. Nearly confluent HUVECs were cultured with MCDB131 supplemented with 100 µg/ml heparin and 0.1% BSA (MCDB131/heparin/BSA) for 18 h. After this serum-deprivation, they were further incubated in MCDB131/heparin/BSA with or without inostamycin (250 ng/ml) for 1 h. Cells were harvested, resuspended in MCDB131/heparin/BSA with or without inostamycin (250 ng/ml) and placed on 0.2% gelatin-pre-coated 8 µm-porous filter in a transwell chamber whose lower compartment has been filled with or without growth factors (10 ng/ml each): VEGF, PDGF, bFGF, or EGF.…”

Section: Transwell Chemotactic Chamber Assaymentioning

confidence: 99%

Inostamycin suppresses vascular endothelial growth factor-stimulated growth and migration of human umbilical vein endothelial cells

Baba

Kato

Mochimatsu

et al. 2004

Clin Exp Metastasis

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Angiogenesis involves multiple steps including proliferation and migration of endothelial cells. In the present study, we determined the effect of inostamycin (an inhibitor of phosphatidylinositol synthesis) on vascular endothelial growth factor (VEGF)-induced proliferation and migration of human umbilical vein endothelial cells (HUVECs). Inostamycin significantly attenuated both VEGF-induced proliferation and migration of HUVECs. Inostamycin inhibited activation of mitogen-activated kinases (ERK and p38) and elevation of cyclin D1 induced by VEGF. These data suggest that inostamycin reduced both proliferation and migration of HUVECs by targeting ERK-cyclin D1 and p38, respectively.

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Stimulation of Motility of Human Renal Cell Carcinoma by SPARC/Osteonectin/BM-40 Associated with Type IV Collagen

Cited by 18 publications

References 29 publications

High production of SPARC/osteonectin/BM-40 in mouse metastatic B16 melanoma cell lines

High production of SPARC/osteonectin/BM-40 in mouse metastatic B16 melanoma cell lines

Endogenous Osteonectin/SPARC/BM-40 Expression Inhibits MDA-MB-231 Breast Cancer Cell Metastasis

Inostamycin suppresses vascular endothelial growth factor-stimulated growth and migration of human umbilical vein endothelial cells

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