ArticleThe American journal of pathology2003
The combination of calmodulin antagonists and interferon-gamma induces apoptosis through caspase-dependent and -independent pathways in cholangiocarcinoma cells.
Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 33 citations in OpenAlex.
- Tafazzin mediates tamoxifen resistance by regulating cellular phospholipid composition in ER-positive breast cancer.Cancer gene therapy · 2024Article
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- Calmodulin antagonists induce cell cycle arrest and apoptosis in vitro and inhibit tumor growth in vivo in human multiple myeloma.BMC cancer · 2014Article
- Tehranolide inhibits cell proliferation via calmodulin inhibition, PDE, and PKA activation.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Structural and biophysical characterization of the interactions between the death domain of Fas receptor and calmodulin.The Journal of biological chemistry · 2013Article
- Article
- Human cholangiocarcinoma development is associated with dysregulation of opioidergic modulation of cholangiocyte growth.Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver · 2009Article
- Genetic and molecular abnormalities in cholangiocarcinogenesis.Anticancer research · 2009Review
- Molecular mechanisms of tamoxifen therapy for cholangiocarcinoma: role of calmodulin.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009Article
- Nervous and Neuroendocrine regulation of the pathophysiology of cholestasis and of biliary carcinogenesis.World journal of gastroenterology · 2006Review
- Point mutations in the C-terminus of HIV-1 gp160 reduce apoptosis and calmodulin binding without affecting viral replication.Virology · 2006Article
- Fas binding to calmodulin regulates apoptosis in osteoclasts.The Journal of biological chemistry · 2005Article
- A peptide inhibitor of cytochrome c/inositol 1,4,5-trisphosphate receptor binding blocks intrinsic and extrinsic cell death pathways.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
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5 authors at 1 institution in 1 country.
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Abstract
Calmodulin (CaM) antagonists have been shown to inhibit tumor cell invasion and metastasis and to induce apoptosis in various tumor models, but the molecular mechanism of CaM antagonist-mediated apoptosis is poorly understood. Here, we demonstrate that interferon (IFN)-gamma induces susceptibility to CaM antagonist-mediated apoptosis in human cholangiocarcinoma cells weakly expressing Fas (Fas-low cells). During CaM antagonist-mediated apoptosis in IFN-gamma-pretreated Fas-low cells, cleavage of caspases-8, -9, and -3 and Bid, release of cytochrome c from the mitochondria and an increase in the free cytosolic calcium concentration were observed. CaM antagonists also caused depolarization of the mitochondrial membrane independent of caspase activation. Although a broad-range caspase inhibitor partially blocked CaM antagonist-mediated apoptosis, the neutralizing Fas antibody had no effect, suggesting that CaM antagonist-mediated apoptosis does not require interaction between CaM antagonists and surface Fas. CaM antagonists induce apoptosis via mechanisms other than inhibition of CaM-dependent protein kinase II and calcineurin, as their inhibitors, KN93 and cyclosporine A, had no effect on apoptosis. Taken together, these results indicate that CaM antagonists induce apoptosis in both caspase-dependent and -independent manners, and that susceptibility to CaM antagonists is modulated by IFN-gamma. The combination of IFN-gamma and CaM antagonists, including tamoxifen, may be a potential therapeutic modality for cholangiocarcinoma and possibly other malignancies.
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