Hepatocyte growth factor—How do I know thee? Let me count the ways

LaBrecque, Douglas R.

doi:10.1016/0016-5085(92)91197-c

Cited by 10 publications

(2 citation statements)

References 55 publications

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“…Of those transgenic mice that express TGF-a, 50± 70 per cent develop hepatocellular tumours by 18 months. In contrast, transgenic mice expressing HGF have no increased incidence of tumours; HGF has actually been found to suppress the growth of many hepatocellular carcinomas in vitro 38,39 .…”

Section: Complete Mitogensmentioning

confidence: 99%

The mystery of liver regeneration

Court

Wemyss‐Holden

Dennison

et al. 2002

British Journal of Surgery

121

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Section: Complete Mitogensmentioning

confidence: 99%

The mystery of liver regeneration

Court

Wemyss‐Holden

Dennison

et al. 2002

British Journal of Surgery

121

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“…All of these cells express the HGF receptor, a member of the tyrosine-kinase family of receptors and recently identified as the product of the c-met proto-oncogene (Bottaro et al, 1991). Thus, because of its potent mitogenic, morphogenic, and motogenic properties (for reviews see LaBrecque, 1992;Michalopoulos and Zarnegar, 1992;Nakamura, 19911, HGF has been implicated in mediating embryonic development (Sonnenberg et al, 1993), cell differentiation (Stern et al, 1990), and organ regeneration after injury (Fujiwara et al, 19!33;Higuchi and Nakamura, 1991;Hu et al, 1993).…”

mentioning

confidence: 99%

Upregulation of molecular motor-encoding genes during hepatocyte growth factor-and epidermal growth factor-induced cell motility

et al. 1996

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Hepatocyte growth factor (HGF) and epidermal growth factor (EGF) are known to stimulate the locomotion of epithelial cells in culture. However, the molecular mechanisms which mediate these important changes are poorly understood. Here we have determined the effects of HGF and EGF on hepatocyte morphology, cytoskeletal organization, and the expression of molecular motor-encoding genes. Primary cultures of hepatocytes were treated with 10 ng/ml of HGF or EGF and observed with phase and fluorescence microscopy at 10, 24, and 48 h after treatment. We found that, over time, treated cells spread and became elongated after 24 h of treatment while forming long processes with dramatic alterations in the microtubule and actin cytoskeletons by 48 h. Quantitative Northern blot analysis was performed to measure expression of cytoskeletal-(beta-actin, alpha-tubulin) and molecular motor-(dynein, kinesin, and myosin I alpha and II) encoding genes which may contribute to this change in form. We observed the highest increase in levels of expression for myosin II (3.3-fold), kinesin (2.7-fold), myosin I alpha (2.2-fold), and alpha-tubulin (1.9-fold) after only 2 h of treatment with HGF. In contrast, EGF upregulated the expression of myosin I alpha (2.4-fold), kinesin (1.5-fold), and dynein (1.5-fold) at 10 h. The expression of the beta-actin gene remained constant in HGF-treated cells, while EGF induced a slight upregulation after 10 h of treatment. These results show for the first time that a selective upregulation of molecular motor-encoding genes correlates with alterations in cell shape and motility induced by HGF and EGF.

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c-met mRNA overexpression in human hepatocellular carcinoma

et al. 1994

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This study was aimed at assessing the presence of c-met overexpression in human hepatocellular carcinoma and at determining whether this feature is associated with a definite clinical or pathological characteristic. Expression of c-met was determined by Northern-blot hybridization of a specific probe (human met proto-oncogene) in 18 tumoral and nontumoral liver samples obtained in 18 cirrhotic patients with hepatocellular carcinoma submitted to surgical treatment. Eight of the 18 hepatocellular carcinomas exhibited c-met overexpression, with an increase ranging between 2-fold and 10-fold when compared by densitometry with the surrounding liver. By contrast, in the remaining 10 cases c-met expression was almost identical to that of the surrounding nontumoral liver tissue. Overexpression of c-met was not related to either the age, sex, etiology or functional status of the underlying liver disease, or to the size of the tumor, to its differentiation degree or to the presence of pseudocapsule invasion and existence of additional neoplastic nodules. These data indicate that almost half of the human hepatocellular carcinomas exhibit c-met overexpression. Nevertheless, the biological relevance of this characteristic is not known.

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Hepatocyte growth factor—How do I know thee? Let me count the ways

Cited by 10 publications

References 55 publications

The mystery of liver regeneration

The mystery of liver regeneration

Upregulation of molecular motor-encoding genes during hepatocyte growth factor-and epidermal growth factor-induced cell motility

c-met mRNA overexpression in human hepatocellular carcinoma

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