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RETRACTED ARTICLE: Hepatocyte growth factor production is stimulated by gangliosides and TGF-β isoforms in human glioma cells

  • Lab. Investigation-Human/Animal Tissue
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This article was retracted on 30 January 2010

This article was retracted on 30 January 2010

Abstract

Hepatocyte growth factor (HGF) is a pleiotrophic cytokine that stimulates motility and invasion of several cancer cell types and induces angiogenesis, which is known to be expressed in several malignancies including glioma. The effect of transforming growth factor-beta (TGF-β) isoforrns as well as gangliosides on HGF production was investigated in human glioma cell lines. TGF-β isoforms and gangliosides were found to differentially stimulate HGF production by these cells. The ganglioside GD3 enhanced this release to the greatest extent and the stimulation was more marked in a glioblastoma cell line than in the two other anaplastic astrocytoma cell lines. These results suggest that both TGF-βs and gangliosides may act as indirect angiogenic factors by stimulating HGF secretion.

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Abbreviations

HGF:

Hepatocyte growth factor

TGF-β:

Transforming growth factor-beta

ELISA:

Enzyme linked immunosorbant assay

DMEM:

Dulbecco’s modified Eagle’s medium

FCS:

Fetal calf serum

SFM:

Serum-free medium

BSA:

Bovine serum albumin

PBS:

Phosphate buffered saline

bFGF:

Basic fibroblast growth factor

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Acknowledgements

We thank professor Hong Wang at Henry Ford Hospital for critical reading of the paper and department of pathology for reviewing the histologic slides with D. **a, Ph.D. This work was supported by a grant JX1B019 from the Hubei Provincial Health Department Foundation of China.

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Correspondence to Sheng-hua Chu.

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This article was retracted at the Editor’s request due to copyright infringement.

An erratum to this article can be found at http://dx.doi.org/10.1007/s11060-010-0120-1

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Chu, Sh., Ma, Yb., Zhang, H. et al. RETRACTED ARTICLE: Hepatocyte growth factor production is stimulated by gangliosides and TGF-β isoforms in human glioma cells. J Neurooncol 85, 33–38 (2007). https://doi.org/10.1007/s11060-007-9387-2

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  • DOI: https://doi.org/10.1007/s11060-007-9387-2

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