ArticlePloS one2013
Activation of Notch signaling is required for cholangiocarcinoma progression and is enhanced by inactivation of p53 in vivo.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 31 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Criteria for preclinical models of cholangiocarcinoma: scientific and medical relevance.Nature reviews. Gastroenterology & hepatology · 2023Guideline
- Molecular Alterations and Pathways in Intrahepatic Cholangiocarcinoma: Available Evidence and New Perspectives.International journal of molecular sciences · 2025Review
- Cellular Origins and Lineage Plasticity in Cancer.Cold Spring Harbor perspectives in medicine · 2024Review
- Atractylodin and β-eudesmol from Atractylodes lancea (Thunb.) DC. Inhibit Cholangiocarcinoma Cell Proliferation by Downregulating the Notch Signaling Pathway.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- KCTD10 functions as a tumor suppressor in hepatocellular carcinoma by triggering the Notch signaling pathway.American journal of translational research · 2023Article
- Notch signaling in the pathogenesis, progression and identification of potential targets for cholangiocarcinoma (Review).Molecular and clinical oncology · 2022Review
- Effects of I125 seed stent implantation combined with arterial infusion chemoembolization on tumor markers, p53 expression, and prognosis in patients with cholangiocarcinoma.Bioengineered · 2022Article
- Cell of origin in biliary tract cancers and clinical implications.JHEP reports : innovation in hepatology · 2021Review
- Notch signalling pathway in development of cholangiocarcinoma.World journal of gastrointestinal oncology · 2020Review
- Review
- Cinobufagin inhibits tumor growth by inducing apoptosis through Notch signaling pathways in human cholangiocarcinoma.Translational cancer research · 2019Article
- The role of tumour microenvironment: a new vision for cholangiocarcinoma.Journal of cellular and molecular medicine · 2019Review
- Article
- YAP Activation Drives Liver Regeneration after Cholestatic Damage Induced byInternational journal of molecular sciences · 2018Article
- ACGH detects distinct genomic alterations of primary intrahepatic cholangiocarcinomas and matched lymph node metastases and identifies a poor prognosis subclass.Scientific reports · 2018Article
- The cholangiocyte primary cilium in health and disease.Biochimica et biophysica acta. Molecular basis of disease · 2018Review
- Molecular Mechanisms Driving Cholangiocarcinoma Invasiveness: An Overview.Gene expression · 2018Review
- Article
- MiR-204 down-regulation elicited perturbation of a gene target signature common to human cholangiocarcinoma and gastric cancer.Oncotarget · 2017Article
- Article
Corrections and comments
- Correction · 2018-11-01Duplication of/in Image · Error in Image · Investigation by Company/Institution ·
- Expression of concern · 2019-12-05Error in Image · Upgrade/Update of Prior Notice(s) ·
- Erratum issued
- Expression of concern
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledCholangiocacinoma (CC) is a cancer disease with rising incidence. Notch signaling has been shown to be deregulated in many cancers. However, the role of this signaling pathway in the carcinogenesis of CC is still not fully explored. In this study, we investigated the effects of Notch inhibition by γ-secretase inhibitor IX (GSI IX) in cultured human CC cell lines and we established a transgenic mouse model with liver specific expression of the intracellular domain of Notch (Notch-ICD) and inactivation of tumor suppressor p53. GSI IX treatment effectively impaired cell proliferation, migration, invasion, epithelial to mesenchymal transition and growth of softagar colonies. In vivo overexpression of Notch-ICD together with an inactivation of p53 significantly increased tumor burden and showed CC characteristics.
conclusionOur study highlights the importance of Notch signaling in the tumorigenesis of CC and demonstrates that additional inactivation of p53 in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.