ArticleCurrent medical science2019
Notch1 Drives the Formation and Proliferation of Intrahepatic Cholangiocarcinoma.
Article in Current medical science, 2019. 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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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Preclinical mouse models for studying cholangiocarcinoma.Liver research (Beijing, China) · 2026Review
- The Impact of Normal Hepatobiliary Cell Zonation Programs on the Phenotypes and Functions of Primary Liver Tumors.Liver cancer · 2025Review
- NOTCH signalling - a core regulator of bile duct disease?Disease models & mechanisms · 2023Review
- Hydrodynamic Delivery: Characteristics, Applications, and Technological Advances.Pharmaceutics · 2023Review
- 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
- Update on Hepatobiliary Plasticity.Seminars in liver disease · 2023Article
- Hes1 Controls Proliferation and Apoptosis in Chronic Lymphoblastic Leukemia Cells by Modulating PTEN Expression.Molecular biotechnology · 2022Article
- Selecting an Appropriate Experimental Animal Model for Cholangiocarcinoma Research.Journal of clinical and translational hepatology · 2022Review
- The Tumor Microenvironment Drives Intrahepatic Cholangiocarcinoma Progression.International journal of molecular sciences · 2022Article
- Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular mechanisms underlying the development of intrahepatic cholangiocarcinoma (ICC) are not clear yet. In this study, we investigated the involvement of Notch1 in the development of ICC. The cDNA microarray analysis showed that Notch1 expression was higher in ICC tissues than in normal biliary epithelial cells. Stable transfection of Notch1 receptor intracellular domain (NICD1) by hydrodynamic tail vein injection induced ICC formation in mice. Western blotting confirmed that Notch1 signaling was activated in human ICC cell lines and mouse ICC tissues. Silencing Notch1 with specific short interfering RNA (siRNA) inhibited the proliferation of ICC cells. Flow cytometry and Western blotting indicated that apoptosis was induced in Notch1-silenced ICC cells compared with controls. Additionally, Notch1 silencing was associated with the inhibition of hairy and enhancer of split-1 (Hes1) and activation of the phosphatase and tensin homolog (PTEN)/p53 pathway. Taken together, these data suggest that Notch1 drives ICC formation and proliferation; downregulation of Notch1 induces apoptosis in ICC cells; Notch1 signaling may serve as a novel therapeutic target for the treatment of ICC.
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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.