ArticlePathology oncology research : POR2010
Arsenic trioxide inhibits cholangiocarcinoma cell growth and induces apoptosis.
Article in Pathology oncology research : POR, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- The ATO/miRNA-885-5p/MTPN axis induces reversal of drug-resistance in cholangiocarcinoma.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- Autophagy as a Potential Therapy for Malignant Glioma.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Arsenic sulfide as a potential anti‑cancer drug.Molecular medicine reports · 2015Article
- Anticancer effect of arsenic trioxide on cholangiocarcinoma: in vitro experiments and in vivo xenograft mouse model.Clinical and experimental medicine · 2014Article
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5 authors at 1 institution in 1 country.
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Abstract
Arsenic trioxide (As(2)O(3)), an ingredient in many traditional Chinese medicines, has drawn broad attention due to its therapeutic effects on a variety of cancers, including some solid tumors. However, the effects of As(2)O(3) on cholangiocarcinoma have not been reported. In the present study, we demonstrate for the first time that clinically obtainable concentrations of As(2)O(3) inhibit cell growth and induce apoptosis in human cholangiocarcinoma SK-ChA-1 cells. As(2)O(3)-induced apoptosis was partially inhibited by caspase inhibitor and accompanied by changes in the expression of Bcl-2 family proteins, decrease of mitochondrial membrane potential (MMP), release of cytochrome C from mitochondria, activation of caspase-3, caspase-9, and cleavage of poly (ADP-ribose) polymerase (PARP). Thus As(2)O(3) induces apoptosis in SK-ChA-1 cells via mitochondria-mediated, caspases-dependent pathways. As(2)O(3) inhibition of Akt phosphorylation may contribute to As(2)O(3)-mediated cholangiocarcinoma cell growth inhibition and apoptosis induction.
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