ArticleThe American journal of pathology1999
Apoptosis and tumorigenesis in human cholangiocarcinoma cells. Involvement of Fas/APO-1 (CD95) and calmodulin.
Article in The American journal of pathology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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.
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Who cites it
22 citing papers in PubMed, 56 citations in OpenAlex.
- Phenothiazine Derivatives and Their Impact on the Apoptosis Processes: A Review.Journal of applied toxicology : JAT · 2026Review
- Hepatic Nuclear Receptors in Cholestasis-to-Cholangiocarcinoma Pathology.The American journal of pathology · 2025Review
- Striatin translocates to the cytosol of apoptotic cells and is proteolytically cleaved in a caspase 3-dependent manner.Heliyon · 2020Article
- Effect of Melatonin and Calmodulin in an Idiopathic Scoliosis Model.BioMed research international · 2016Article
- Article
- Identification and Characterization of the Interaction Site between cFLIPL and Calmodulin.PloS one · 2015Article
- Characterization of calmodulin-Fas death domain interaction: an integrated experimental and computational study.Biochemistry · 2014Article
- Structural and biophysical characterization of the interactions between the death domain of Fas receptor and calmodulin.The Journal of biological chemistry · 2013Article
- Molecular pathogenesis of cholangiocarcinoma.International journal of hepatology · 2012Article
- Article
- Role of sex hormones in the modulation of cholangiocyte function.World journal of gastrointestinal pathophysiology · 2010Article
- The effect of calmodulin antagonists on scoliosis: bipedal C57BL/6 mice model.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2009Article
- Molecular mechanisms of tamoxifen therapy for cholangiocarcinoma: role of calmodulin.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009Article
- Conformation and free energy analyses of the complex of calcium-bound calmodulin and the Fas death domain.Biophysical journal · 2008Article
- ESR1 promoter hypermethylation does not predict atypia in RPFNA nor persistent atypia after 12 months tamoxifen chemoprevention.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2008Article
- Circulating and hepatic Fas expression in HCV-induced chronic liver disease and hepatocellular carcinoma.Medscape journal of medicine · 2008Article
- Fas-mediated apoptosis in cholangiocarcinoma cells is enhanced by 3,3'-diindolylmethane through inhibition of AKT signaling and FLICE-like inhibitory protein.The American journal of pathology · 2006Article
- Nervous and Neuroendocrine regulation of the pathophysiology of cholestasis and of biliary carcinogenesis.World journal of gastroenterology · 2006Review
- Fas binding to calmodulin regulates apoptosis in osteoclasts.The Journal of biological chemistry · 2005Article
- The combination of calmodulin antagonists and interferon-gamma induces apoptosis through caspase-dependent and -independent pathways in cholangiocarcinoma cells.The American journal of pathology · 2003Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
We have previously demonstrated that tamoxifen inhibits the growth of human cholangiocarcinoma cells in culture and inhibits tumor growth when cells are injected into nude mice. However, the mechanism of action of tamoxifen remains unknown. Here we demonstrate that tamoxifen and trifluoperazine, both potent calmodulin antagonists, induce apoptosis in vitro, probably acting via the Fas system, in human cholangiocarcinoma cells. Human cholangiocarcinoma cell lines heterogeneously express Fas antigen on their surface. Fas-negative and Fas-positive surface-expressing cells were isolated, cloned, and cultured. Fas antibody, tamoxifen, and trifluoperazine induced dose-dependent apoptosis only in Fas-positive cells; Fas-negative cells were unaffected. Furthermore, apoptosis induced by tamoxifen in Fas-positive cells was blocked by an inhibitory Fas antibody. Tamoxifen was not acting through an anti-estrogenic mechanism, because neither Fas-negative nor Fas-positive cells expressed estrogen receptors and the pure anti-estrogen compound, ICI 182780, did not induce apoptosis in either cell line. Fas-negative cells, but not Fas-positive cells, were able to produce tumors when subcutaneously injected into nude mice. These findings suggest Fas may be a candidate oncogene involved in the pathogenesis of cholangiocarcinoma. Furthermore, the similarity between the pro-apoptotic effects of tamoxifen and trifluoperazine support an underlying molecular mechanism for Fas-mediated apoptosis that involves calmodulin.
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