Hepatocyte growth factor induces pro-apoptotic genes in HepG2 hepatoma but not in B16-F1 melanoma cells

Matteucci, Emanuela; Castoldi, Raffaella; Desiderio, Maria Alfonsina

doi:10.1002/1097-4652(2000)9999:9999<000::aid-jcp1033>3.0.co;2-8

Cited by 25 publications

(20 citation statements)

References 63 publications

(91 reference statements)

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“…Liver and lung myofibroblasts 60,61 Mouse sarcoma cell lines Sarcoma-180 and Meth A 42,43,45,[62][63][64][65] Transformed rat liver epithelial cell lines 66 Mouse hepatocarcinoma cell lines Hepa 1 and Hepa 1-6 67,68 Human hepatoblastoma cell line HepG2 69,70 Ovarian carcinoma cells 71,72 (HGF and Paclitaxel or Cisplatin) Human breast carcinoma cells lines MCF-7 and MDA-MB-231 70 The HGF/SF induces efficient survival of many cell types against various stress conditions or apoptotic inducer. In contrast, in other cell lines, HGF/SF stimulation induces apoptotic cell death, illustrating opposite properties of HGF/SF-MET according to the cell type…”

Section: Cell Type Referencesmentioning

confidence: 88%

The shadow of death on the MET tyrosine kinase receptor

Tulasne

Foveau

2007

Cell Death Differ

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The MET tyrosine kinase receptor is a high-affinity receptor for hepatocyte growth factor/scatter factor (HGF/SF). HGF/SF-MET system is necessary for embryonic development, and aberrant MET signalling favours tumorigenesis and metastasis. MET is a prototype of tyrosine kinase receptor, which is able to counteract apoptosis through the initiation of a survival signal involving notably the PI3K-Akt pathway. Paradoxically, the MET receptor is also able to promote apoptosis when activated by HGF/SF or independently of ligand stimulation. The molecular mechanisms underlying this uncommon response have been recently investigated and revealed dual antiapoptotic or proapoptotic property of MET according to the cell type or stress conditions. Although the involvement of MET in the regulation of integrated biological responses mostly took into account its efficient antiapoptotic function, its proapoptotic responses could also be important for regulation of the survival/apoptosis balance and play a role during the development or tumour progression.

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Section: Cell Type Referencesmentioning

confidence: 88%

The shadow of death on the MET tyrosine kinase receptor

Tulasne

Foveau

2007

Cell Death Differ

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“…This observation may explain why HGF only acts as a mitogen in vivo when there is loss of cell-cell contact [37]. It also helps to reconcile many contradictory reports in the literature regarding the effect of HGF on growth both in vitro and in vivo [14][15][16][17][18][19][20][21][22][23]31,38]. In the current work we examined the influence of HGF on GSH status because GSH is another parameter known to influence hepatocyte growth.…”

Section: Discussionmentioning

confidence: 99%

“…HGF has been reported to either activate JNK [30][31][32] or inhibit JNK [33] and to be either proapoptotic [20,31,32] or anti-apoptotic [33,34]. TNFα is known to induce apoptosis via sustained JNK activation [35,36].…”

Section: Molecular Mechanism Of Cell Density's Influence On Hgf's Apomentioning

confidence: 99%

“…It induced growth at low cell density whereas it induced albumin synthesis at high cell density [13]. The role of HGF in liver cancer has been highly controversial [14][15][16][17] and its effect in liver cancer cells often contradictory [18][19][20][21][22][23]. Recently, we reported that the effect of HGF in liver cancer cell line HepG2 depends on the cell density [24].…”

Section: Introductionmentioning

confidence: 99%

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Effects of hepatocyte growth factor on glutathione synthesis, growth, and apoptosis is cell density-dependent

Yang¹,

Magilnick²,

Xia³

et al. 2008

Experimental Cell Research

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Hepatocyte growth factor (HGF) is a potent hepatocyte mitogen that exerts opposing effects depending on cell density. Glutathione (GSH) is the main non-protein thiol in mammalian cells that modulates growth and apoptosis. We previously showed that GSH level is inversely related to cell density of hepatocytes and is positively related to growth. Our current work examined whether HGF can modulate GSH synthesis in a cell density dependent manner and how GSH in turn influence HGF's effects. We found HGF treatment of H4IIE cells increased cell GSH levels only under subconfluent density. The increase in cell GSH under low density was due to increased transcription of GSH synthetic enzymes. This correlated with increased protein levels and nuclear binding activities of c-Jun, c-Fos, p65, p50, Nrf1 and Nrf2 to the promoter region of these genes. HGF acts as a mitogen in H4IIE cells under low cell density and protects against tumor necrosis factor α (TNFα)-induced apoptosis by limiting JNK activation. However, HGF is pro-apoptotic under high cell density and exacerbates TNFα-induced apoptosis by potentiating JNK activation. The increase in cell GSH under low cell density allows HGF to exert its full mitogenic effect but is not necessary for its anti-apoptotic effect.

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“…The survival role of HGF has been observed in a number of cancer types, such as breast carcinoma, glioblastoma, and leiomyosarcoma cells (11,(17)(18)(19)(20). Nonetheless, in some experimental conditions, HGF-mediated cytotoxicity has been reported (21)(22)(23)(24).…”

Section: Introductionmentioning

confidence: 99%

Hepatocyte Growth Factor Sensitizes Human Ovarian Carcinoma Cell Lines to Paclitaxel and Cisplatin

et al. 2004

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The hepatocyte growth factor (HGF) receptor, encoded by the MET oncogene, is expressed in ϳ70% of human ovarian carcinomas and overexpressed in 30% of cases. Because HGF is known to protect cells from apoptosis, we investigated whether receptor expression modifies ovarian cancer cell response to chemotherapy. The apoptotic effect of the frontline chemotherapeutic drugs paclitaxel and cisplatin on cells treated with HGF was studied. In ovarian cancer cell lines, pretreatment with HGF surprisingly enhances the apoptotic response to low doses of paclitaxel and cisplatin. HGF empowers specifically the intrinsic apoptotic pathway, whereas it protects cells from extrinsic Fas-induced apoptosis. Chemotherapy sensitization is specific for HGF because another growth factor (e.g., epidermal growth factor) increases ovarian cancer cell survival. In nonovarian cancer cell models, as expected, HGF provides protection from drug-induced apoptosis. These data show that HGF sensitizes ovarian carcinoma cells to low-dose chemotherapeutic agents. This suggests that HGF may be used to improve response to chemotherapy in a set of human ovarian carcinomas molecularly classified based on the MET oncogene expression.

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Hepatocyte growth factor induces pro-apoptotic genes in HepG2 hepatoma but not in B16-F1 melanoma cells

Cited by 25 publications

References 63 publications

The shadow of death on the MET tyrosine kinase receptor

The shadow of death on the MET tyrosine kinase receptor

Effects of hepatocyte growth factor on glutathione synthesis, growth, and apoptosis is cell density-dependent

Hepatocyte Growth Factor Sensitizes Human Ovarian Carcinoma Cell Lines to Paclitaxel and Cisplatin

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