ArticleThe American journal of pathology2009
Up-regulation of Bcl-xl by hepatocyte growth factor in human mesothelioma cells involves ETS transcription factors.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 20 citations in OpenAlex.
- Aberrant Bcl-x splicing in cancer: from molecular mechanism to therapeutic modulation.Journal of experimental & clinical cancer research : CR · 2021Review
- Mechanism of inhibition of Shiga-toxigenicCell death discovery · 2018Article
- Erythroblast transformation-specific 2 correlates with vascular smooth muscle cell apoptosis in rat heterotopic heart transplantation model.Journal of thoracic disease · 2016Article
- ETS2 mediated tumor suppressive function and MET oncogene inhibition in human non-small cell lung cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013Article
- Nrf2-induced antiapoptotic Bcl-xL protein enhances cell survival and drug resistance.Free radical biology & medicine · 2013Article
- Article
- The downregulation of Mcl-1 via USP9X inhibition sensitizes solid tumors to Bcl-xl inhibition.BMC cancer · 2012Article
- The possible functions of duplicated ets (GGAA) motifs located near transcription start sites of various human genes.Cellular and molecular life sciences : CMLS · 2011Article
- Genes associated with prognosis after surgery for malignant pleural mesothelioma promote tumor cell survival in vitro.BMC cancer · 2011Article
- Novel therapy for myocardial infarction: can HGF/Met be beneficial?Cellular and molecular life sciences : CMLS · 2011Review
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Authors and funding
9 authors at 2 institutions in 1 country.
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Abstract
Bcl-xl and the hepatocyte growth factor (HGF) receptor c-Met are both highly expressed in mesotheliomas, where they protect cells from apoptosis and can confer resistance to conventional therapeutic agents. In our current study, we investigate a model for the transcriptional control of Bcl-xl that involves ETS transcription factors and the HGF/Met axis. In addition, the effects of activated c-Met on the phosphorylation of the ETS family transcriptional factors were examined. The transient expression of ETS-2 and PU.1 cDNAs in mesothelioma cell lines resulted in an increase in the promoter activity of Bcl-xl and consequently in its mRNA and protein expression levels, whereas the transcriptional repressor Tel suppressed Bcl-xl transcription. The activation of the HGF/Met axis led to rapid phosphorylation of ETS family transcription factors in mesothelioma cells through the mitogen-activated protein kinase pathway and via nuclear accumulation of ETS-2 and PU.1. A chromatin immunoprecipitation assay further demonstrated that the activation of c-Met enhanced the binding of ETS transcriptional factors to the Bcl-x promoter. Finally, we determined the Bcl-xl and phosphorylated c-Met expression levels in mesothelioma patient samples; these data suggest a strong correlation between Bcl-xl and phosphorylated c-Met levels. Taken together, these findings support a role for c-Met as an inhibitor of apoptosis and an activator of Bcl-xl.
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