ArticleJournal of molecular histology2011
Cooperation of deregulated Notch signaling and Ras pathway in human hepatocarcinogenesis.
Article in Journal of molecular histology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
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- Activation of signal transduction pathways during hepatic oncogenesis.Cancer letters · 2016Article
- Synergistic function of Kras mutation and HBx in initiation and progression of hepatocellular carcinoma in mice.Oncogene · 2014Article
- Expression of TSG101 protein and LSF transcription factor in HPV-positive cervical cancer cells.Oncology letters · 2014Article
- OncomiRdbB: a comprehensive database of microRNAs and their targets in breast cancer.BMC bioinformatics · 2014Article
- AhR expression is increased in hepatocellular carcinoma.Journal of molecular histology · 2013Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant Notch signaling and Ras pathway had been highlighted a potential role for in human cancers. Yet, relatively little was known about the roles of wild type Notch signaling and Ras in human hepatocarcinogenesis. The aim of this study was to investigate the roles of Ras-Notch signaling cooperation in hepatic cells transformation and proliferation. Hepatocellular carcinoma specimens from 25 patients were analyzed for Notch-1, Ras and Late Simian Virus 40 Factor (LSF) expression using immunohistochemistry. Results showed that Notch-1(76%, 19/25, P < 0.0001), Ras (40%, 10/25, P < 0.01) and LSF (84%, 21/25, P < 0.0001) were significantly up-regulated in hepatocellular carcinoma compared with non-cancer samples. The correlations between the expression and the biological effects of Notch1 and Ras were analyzed by genetic and pharmacological methods. Constitutively active Notch1 alone failed to transform immortalized L02 cells in vivo, it synergized with the Ras pathway to promote hepatic cells transformation. However, their cooperation increased the levels of LSF mRNA and protein, which stimulates L02 cells proliferation. These results exhibited highly aggressive progression, suggesting that Notch-Ras cooperation maybe lead to poor prognosis. Thus, combining the inhibition of the two pathways provided an attractive avenue for therapeutic intervention to overcome this advanced disease.
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