Effect of Geldanamycin on the Glioma Cell Invasion Induced by Hepatocyte Growth Factor

To investigate the effect of geldanamycin (GDM) on the invasion ability of glioma cell induced by hepatocyte growth factor (HGF). Malignant glioma cell line U251-MG and U87-MG were cultured’and the capability of cell invasion was detected using a Transwell culture system. HGF significantly promoted the invasion ability of both U251-MG and U87-MG cells as compared with the normal control (NC) (P < 0.05). Forty eight hours after GDM treatment, the invasive growth of glioma cells was significantly decreased as compared with either NC or HGF group (P < 0.05). When cells were exposed to GDM plus HGF for 48 h, the cell invasion capability was greatly reduced as compared with either NC or HGF group (P < 0.05). The number of invaded cells in GDM plus HGF group was similar to that of GDM group.GDM can inhibit the invasion ability of glioma cells induced by HGF.

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CXCR4 and SDF-1 Production Are Stimulated by Hepatocyte Growth Factor and Promote Glioma Cell Invasion

Onkologie ◽

10.1159/000216352 ◽

2009 ◽

Vol 32 (6) ◽

pp. 331-336 ◽

Cited By ~ 20

Author(s):

Hanjun Tu ◽

Zhangming Zhou ◽

Qingle Liang ◽

Zhiqiang Li ◽

Dongsheng Li ◽

...

Keyword(s):

Growth Factor ◽

Hepatocyte Growth Factor ◽

Cell Invasion ◽

Glioma Cell ◽

Hepatocyte Growth

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Tumor-derived hepatocyte growth factor is associated with poor prognosis of patients with glioma and influences the chemosensitivity of glioma cell line to cisplatin in vitro

World Journal of Surgical Oncology ◽

10.1186/1477-7819-10-128 ◽

2012 ◽

Vol 10 (1) ◽

pp. 128 ◽

Cited By ~ 5

Author(s):

You-feng Guo ◽

Xiao-bing Wang ◽

Xiao-ying Tian ◽

Yang Li ◽

Bin Li ◽

...

Keyword(s):

Growth Factor ◽

Hepatocyte Growth Factor ◽

Cell Line ◽

Poor Prognosis ◽

Glioma Cell ◽

Glioma Cell Line ◽

Hepatocyte Growth

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HGF Converts ErbB2/Neu Epithelial Morphogenesis to Cell Invasion

Molecular Biology of the Cell ◽

10.1091/mbc.e04-07-0567 ◽

2005 ◽

Vol 16 (2) ◽

pp. 550-561 ◽

Cited By ~ 77

Author(s):

Hanane Khoury ◽

Monica A. Naujokas ◽

Dongmei Zuo ◽

Veena Sangwan ◽

Melanie M. Frigault ◽

...

Keyword(s):

Growth Factor ◽

Hepatocyte Growth Factor ◽

Cell Invasion ◽

Single Cells ◽

Epithelial Morphogenesis ◽

Cell Junctions ◽

Junction Protein ◽

Hepatocyte Growth ◽

E Cadherin ◽

Cell Cell

Activation of the hepatocyte growth factor receptor Met induces a morphogenic response and stimulates the formation of branching tubules by Madin-Darby canine kidney (MDCK) epithelial cells in three-dimensional cultures. A constitutively activated ErbB2/Neu receptor, NeuNT, promotes a similar invasive morphogenic program in MDCK cells. Because both receptors are expressed in breast epithelia, are associated with poor prognosis, and hepatocyte growth factor (HGF) is expressed in stroma, we examined the consequence of cooperation between these signals. We show that HGF disrupts NeuNT-induced epithelial morphogenesis, stimulating the breakdown of cell-cell junctions, dispersal, and invasion of single cells. This correlates with a decrease in junctional proteins claudin-1 and E-cadherin, in addition to the internalization of the tight junction protein ZO-1. HGF-induced invasion of NT-expressing cells is abrogated by pretreatment with a pharmacological inhibitor of the mitogen-activated protein kinase kinase (MEK) pathway, which restores E-cadherin and ZO-1 at cell-cell junctions, establishing the involvement of MEK-dependent pathways in this process. These results demonstrate that physiological signals downstream from the HGF/Met receptor synergize with ErbB2/Neu to enhance the malignant phenotype, promoting the breakdown of cell-cell junctions and enhanced cell invasion. This is particularly important for cancers where ErbB2/Neu is overexpressed and HGF is a physiological growth factor found in the stroma.

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