LPA-induced epithelial ovarian cancer (EOC) in vitro invasion and migration are mediated by VEGF receptor-2 (VEGF-R2)

So, John; Wang, Fengqiang; Navari, Jason R.; Schreher, Jeremy; Fishman, David A.

doi:10.1016/j.ygyno.2005.03.004

Cited by 77 publications

(53 citation statements)

References 34 publications

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“…LPA promotes ovarian tumor development through increased cyclin D expression (Chappell et al, 2001). LPA also increases vascular endothelial growth factor production, which stimulates angiogenesis (So et al, 2005). In a colon cancer cell line, LPA increases the synthesis of macrophage migration inhibitory factor, which promotes tumor growth (Sun et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Autotaxin protects MCF-7 breast cancer and MDA-MB-435 melanoma cells against Taxol-induced apoptosis

et al. 2008

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Section: Introductionmentioning

confidence: 99%

Autotaxin protects MCF-7 breast cancer and MDA-MB-435 melanoma cells against Taxol-induced apoptosis

et al. 2008

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“…We and others have shown that LPA stimulates the migration and invasion of ovarian cancer cells (10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22). Although most, if not all, of these studies were conducted in established ovarian cancer cell lines, we have recently conducted LPA-and S1P-induced cell migration and invasion experiments in primary EOC and nonmalignant human ovarian surface epithelial cells (11,23).…”

Section: Introductionmentioning

confidence: 99%

Lysophosphatidic acid stimulates cell migration, invasion, and colony formation as well as tumorigenesis/metastasis of mouse ovarian cancer in immunocompetent mice

Wang

Zhang

et al. 2009

Molecular Cancer Therapeutics

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We have already established human xenographic models for the effect of lysophosphatidic acid (LPA) on tumor metastasis in vivo. The purpose of this work is to establish a preclinical LPA effect model in immunocompetent mice. We first characterized the mouse epithelial ovarian cancer (EOC) cell line ID8 for its responsiveness to LPA in cell proliferation, migration, and invasion and compared these properties with those of human EOC. The signaling pathways related to cell migration were further investigated using pharmacologic and genetic approaches. The effects of LPA on the tumorigenesis of ID8 cells and mouse survival were then examined using two different mouse models (i.p. and orthotopic injections). LPA stimulated cell proliferation, migration, and invasion of mouse EOC ID8 cells in a manner closely resembling its activity in human EOC cells. The signaling pathways involved in LPAinduced cell migration in ID8 cells were also similar to those identified in human EOC cells. We have identified cyclooxygenase-1 and 15-lipoxygenase as two new signaling molecules involved in LPA-induced cell migration in both human and mouse EOC cells. In addition, LPA enhanced the tumorigenesis/metastasis of ID8 cell in vivo as assessed by increased tumor size, early onset of ascites formation, and reduced animal survival. We have established the first LPA-EOC preclinical model in immunocompetent mice. Because ID8 cells respond to LPA similar to human EOC cells, this model is very valuable in developing and testing therapeutic reagents targeting LPA in

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“…The EOC metastatic cascade consists of cellular migration, ECM degradation, proliferation, adhesion, membrane vesicle formation, invasion, and angiogenesis, which are uniquely influenced by the bioactive lipid LPA (42,43,46,47,49,50,(53)(54)(55). LPA has been proposed as a biomarker for ovarian cancer, with several studies showing that plasma levels were elevated in patients with ovarian cancer (49,56,57).…”

Section: Discussionmentioning

confidence: 99%

“…In the present study, we evaluated the correlation of MMP-7 expression to EOC invasiveness by transfection of the MMP-7 sense and antisense gene into DOV13 cells. We further investigated whether MMP-7 secretion and activity are regulated by lysophosphatidic acid (LPA), a bioactive lipid growth factor that is found to be elevated in the plasma and malignant effusions of the majority of women with EOC (98%) and also promotes EOC metastasis (42).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Matrilysin Expression by Antisense or RNA Interference Decreases Lysophosphatidic Acid–Induced Epithelial Ovarian Cancer Invasion

Wang

Smicun

Calluzzo

et al. 2006

Molecular Cancer Research

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Our previous reports show that matrilysin [matrix metalloproteinase (MMP)-7] is overexpressed in epithelial ovarian cancer (EOC) and recombinant MMP-7 promotes EOC invasion in vitro. In the present study, we further evaluated the correlation of MMP-7 expression to EOC invasiveness and examined its role in lysophosphatidic acid (LPA)-induced invasion. By sense and antisense gene transfection in vitro, we show that overexpression of MMP-7 in all MMP-7 stably transfected DOV13 clones significantly enhanced their invasiveness, although MMP-7 antisense transfection caused a 91% decrease of MMP-7 expression (P < 0.01) and 87% decrease of invasion (P < 0.05) in geneticin (G418)-selected DOV13 clone P47-M7As-3 compared with vector-transfected control.As assessed by MMP-7 ELISA, LPA treatment at 10 to 80 Mmol/L significantly stimulated the secretion of total MMP-7 in DOV13 conditioned medium (P < 0.01). In addition, LPA apparently induced the activation of MMP-7 in DOV13 cells as detected by gelatin zymography. In the antisense MMP-7-transfected DOV13 clone (P47-M7As-3), LPA-increased invasion was significantly decreased compared with vector control. Moreover, knocking down of MMP-7 by small interfering RNA also suppressed LPA-induced invasion in two EOC cell lines (DOV13 and R182). Altogether, our results show that MMP-7 expression is correlated with EOC invasiveness and LPA-induced MMP-7 secretion/ activation may represent a new mechanism that facilitates ovarian cancer invasion besides the well-known induction of MT1-MMP-mediated proMMP-2 activation by LPA. (Mol Cancer Res 2006;4(11):831 -41)

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LPA-induced epithelial ovarian cancer (EOC) in vitro invasion and migration are mediated by VEGF receptor-2 (VEGF-R2)

Cited by 77 publications

References 34 publications

Autotaxin protects MCF-7 breast cancer and MDA-MB-435 melanoma cells against Taxol-induced apoptosis

Autotaxin protects MCF-7 breast cancer and MDA-MB-435 melanoma cells against Taxol-induced apoptosis

Lysophosphatidic acid stimulates cell migration, invasion, and colony formation as well as tumorigenesis/metastasis of mouse ovarian cancer in immunocompetent mice

Inhibition of Matrilysin Expression by Antisense or RNA Interference Decreases Lysophosphatidic Acid–Induced Epithelial Ovarian Cancer Invasion

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