Expression of HGF/SF in mesothelioma cell lines and its effects on cell motility, proliferation and morphology

Harvey, P; Warn, A.; Dobbin, S; Arakaki, Naokatu; Daikuhara, Yasushi; Jaurand, Marie‐Claude; Warn, R. M.

doi:10.1038/bjc.1998.176

Cited by 40 publications

(39 citation statements)

References 39 publications

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“…The establishment of an autocrine circuit for growth factors frequently confers a selective advantage to tumor cells as well. In particular, the occurrence of an HGF͞Met autocrine loop has been reported in a number of cancers, including MM (16). Moreover, in MDCK, the expression of recombinant Tag has been reported to induce dissociation and motility (30).…”

Section: Discussionmentioning

confidence: 99%

“…Several studies investigated the potential involvement of other growth factors, like platelet-derived growth factor A and B (13), insulin-like growth factor-1 (14), transforming growth factor ␤, fibroblast growth factor-2 (15), and hepatocyte growth factor (HGF) (16)(17)(18)(19) in the onset of MM. High levels of HGF, in particular, were detected in pleural effusion from patients with MM (20).…”

Section: Alignant Mesothelioma (Mm) Is An Aggressive and Invasivementioning

confidence: 99%

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SV40 replication in human mesothelial cells induces HGF/Met receptor activation: A model for viral-related carcinogenesis of human malignant mesothelioma

Cacciotti

Libener

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

134

137

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Section: Discussionmentioning

confidence: 99%

Section: Alignant Mesothelioma (Mm) Is An Aggressive and Invasivementioning

confidence: 99%

SV40 replication in human mesothelial cells induces HGF/Met receptor activation: A model for viral-related carcinogenesis of human malignant mesothelioma

Cacciotti

Libener

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

134

137

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“…Transforming growth factor (TGF)-␣ determination in the media of NSCLC cells was performed similarly to a previously described method for detecting hepatocyte growth factor (9). For the determination of TGF-␣, enzyme-linked immunosorbent assays were performed according to the manufacturer's recommended procedures (human TGF-␣ immunoassay; Quantikine; R&D Systems, Minneapolis, MN).…”

Section: Methodsmentioning

confidence: 99%

Gefitinib Induces Apoptosis in the EGFRL858R Non–Small-Cell Lung Cancer Cell Line H3255

Tracy

Mukohara²,

Hansen³

et al. 2004

Cancer Research

331

252

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Somatic mutations in the tyrosine kinase domain of the epidermal growth factor receptor (EGFR) have recently been described in patients with non-small-cell lung cancer (NSCLC) who achieve radiographic regressions to the EGFR inhibitor gefitinib. One of these mutations, L858R (Leu3 Arg), is also found in NSCLC cell line H3255, which is very sensitive to gefitinib treatment. We characterized nine NSCLC cell lines (three isolated from patients with bronchioloalveolar carcinoma and six isolated from patients with adenocarcinoma) for their in vitro sensitivity to gefitinib. Of these, only H3255 (EGFR L858R ) and H1666 (EGFR

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“…Although the mechanisms of development of MM are obscure, the initiation of signaling events after interaction with asbestos fibers may govern transactivation of genes governing cell proliferation and transformation (4). Cell survival, proliferation, and progression of MMs are complex and may be related to overexpression of several autocrine growth factors, including insulin-like growth factor (5, 6), platelet-derived growth factor (7), fibroblast growth factor (8), transforming growth factor b (8), and hepatocyte growth factor/scatter factor (HGF) (9).…”

mentioning

confidence: 99%

HGF Mediates Cell Proliferation of Human Mesothelioma Cells through a PI3K/MEK5/Fra-1 Pathway

Ramos-Niño

Blumen²,

Sabo‐Attwood³

et al. 2008

Am J Respir Cell Mol Biol

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The ligand hepatocyte growth factor/scatter factor (HGF) and its receptor tyrosine kinase, c-Met, are highly expressed in most human malignant mesotheliomas (MMs) and may contribute to their increased growth and viability. Based upon our observation that RNA silencing of fos-related antigen 1 (Fra-1) inhibited c-met expression in rat mesotheliomas (1), we hypothesized that Fra-1 was a key player in HGF-induced proliferation in human MMs. In three of seven human MM lines evaluated, HGF increased Fra-1 levels and phosphorylation of both extracellular signal-regulated kinase 5 (ERK5) and AKT that were inhibited by the phosphatidylinositol 3-kinase (PI3K) inhibitor, LY290042. HGF-dependent phosphorylation and Fra-1 expression were decreased after knockdown of Fra-1, whereas overexpression of Fra-1 blocked the expression of mitogen/extracellular signal-regulated kinase kinases (MEK)5 at the mRNA and protein levels. Stable MM cell lines using a dnMEK5 showed that basal Fra-1 levels were increased in comparison to empty vector control lines. HGF also caused increased MM cell viability and proliferating cell nuclear antigen (PCNA) expression that were abolished by knockdown of MEK5 or Fra-1. Data suggest that HGF-induced effects in some MM cells are mediated via activation of a novel PI3K/ERK5/Fra-1 feedback pathway that might explain tumor-specific effects of c-Met inhibitors on MM and other tumors.Keywords: hepatocyte growth factor/scatter factor; fos-related antigen 1; phosphatidylinositol 3-kinase; MEK5; mesothelioma Malignant mesothelioma (MM) is an insidious tumor associated historically with occupational exposure to asbestos (2, 3). The average survival of patients with MM is less than 1 year after initial diagnosis, and no successful treatment options exist. Although the mechanisms of development of MM are obscure, the initiation of signaling events after interaction with asbestos fibers may govern transactivation of genes governing cell proliferation and transformation (4). Cell survival, proliferation, and progression of MMs are complex and may be related to overexpression of several autocrine growth factors, including insulin-like growth factor (5, 6), platelet-derived growth factor (7), fibroblast growth factor (8), transforming growth factor b (8), and hepatocyte growth factor/scatter factor (HGF) (9).Increased expression of Fos/Jun family members and activator protein-1 (AP-1) transactivation are observed in mesothelial cells after exposure to asbestos and erionite fibers in contrast to other nonpathogenic fibers and particles (10-12). In comparison to other fos/jun mRNAs, fos-related antigen 1 (fra-1) expression is more protracted and critical to expession of c-met and cd44 in a rat model of mesothelial cell transformation (1).Although HGF and its receptor, c-Met, are known to be involved in chemotaxis, growth, and invasion of a number of tumor types including MMs (13-15), the mechanisms of HGF/ Met signaling and their functional ramifications in MMs remain unclear. We previously reported that HGF stimula...

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Expression of HGF/SF in mesothelioma cell lines and its effects on cell motility, proliferation and morphology

Cited by 40 publications

References 39 publications

SV40 replication in human mesothelial cells induces HGF/Met receptor activation: A model for viral-related carcinogenesis of human malignant mesothelioma

SV40 replication in human mesothelial cells induces HGF/Met receptor activation: A model for viral-related carcinogenesis of human malignant mesothelioma

Gefitinib Induces Apoptosis in the EGFRL858R Non–Small-Cell Lung Cancer Cell Line H3255

HGF Mediates Cell Proliferation of Human Mesothelioma Cells through a PI3K/MEK5/Fra-1 Pathway

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