Effect of deoxycholic acid on Ca2+ movement, cell viability and apoptosis in human gastric cancer cells. (February 2015)

• Record Type: Journal Article
• Authors: Chien, Jau-Min; Chou, Chiang-Ting; Liang, Wei-Zhe; Cheng, Jin-Shiung; Chang, Hong-Tai; Tseng, Hui-Wen; Kuo, Soong-Yu; Kuo, Chun-Chi; Chen, Fu-An; Shieh, Pochuen; Ho, Chin-Man; Lin, Jia-Rong; Kuo, Daih-Huang; Jan, Chung-Ren
• Is Part Of: Toxicology mechanisms and methods. Volume 25:Number 2(2015)
• Page Start: 113
• Page End: 119
• Publication Date: 2015-02
• Subjects: Analytical toxicology -- Periodicals; Toxicology -- Periodicals; Toxicology -- Methodology -- Periodicals; 615.907
• DOI: 10.3109/15376516.2014.990597
• Languages: English
• ISSNs: 1537-6516

Abstract

<abstract> <title>Abstract</title> <p>Deoxycholic acid (DOA) is one of the secondary bile acids used as a mild detergent for the isolation of membrane associated proteins. This study examined whether the secondary bile acid, DOA, altered Ca<sup>2+</sup> movement, cell viability and apoptosis in SCM1 human gastric cancer cells. The Ca<sup>2+</sup>-sensitive fluorescent dye fura-2 was used to measure [Ca<sup>2+</sup>]<sub>i</sub>. DOA-evoked [Ca<sup>2+</sup>]<sub>i</sub> rises concentration dependently. The response was reduced by removing extracellular Ca<sup>2+</sup>. DOA-evoked Ca<sup>2+</sup> entry was inhibited by store-operated Ca<sup>2+</sup> channel inhibitors (nifedipine, econazole and SKF96365), the protein kinase C (PKC) activator phorbol 12-myristate 13 acetate (PMA) and the PKC inhibitor GF109203X. In Ca<sup>2+</sup>-free medium, treatment with the endoplasmic reticulum Ca<sup>2+</sup> pump inhibitor thapsigargin (TG) abolished DOA-evoked [Ca<sup>2+</sup>]<sub>i</sub> rises. Conversely, treatment with DOA abolished TG-evoked [Ca<sup>2+</sup>]<sub>i</sub> rises. Inhibition of phospholipase C with U73122 abolished DOA-evoked [Ca<sup>2+</sup>]<sub>i</sub> rises. At 100–500 μM, DOA decreased cell viability, which was not changed by chelating cytosolic Ca<sup>2+</sup> with 1, 2-bis(2-aminophenoxy)ethane-<italic>N, N, N</italic>′, <italic>N</italic>′-tetraacetic acid-acetoxymethyl ester (BAPTA/AM). DOA between 100 and 300 μM also induced apoptosis. Collectively, in SCM1 cells, DOA-induced [Ca<sup>2+</sup>]<sub>i</sub> rises by evoking phospholipase C-dependent Ca<sup>2+</sup> release from the endoplasmic reticulum and Ca<sup>2+</sup> entry via store-operated Ca<sup>2+</sup> channels. DOA also caused Ca<sup>2+</sup>-independent apoptosis.</p> </abstract>