Requirement for store-operated calcium entry in sodium butyrate-induced apoptosis in human colon cancer cells. Issue 1 (10th October 2011)

• Record Type: Journal Article
• Authors: Sun, Suxia; Li, Wenjun; Zhang, He; Zha, Longying; Xue, Yong; Wu, Xianbo; Zou, Fei
• Is Part Of: Bioscience reports. Volume 32:Issue 1(2012)
• Page Start: 83
• Page End: 90
• Publication Date: 2011-10-10
• Subjects: apoptosis -- Ca2+ -- colon cancer cell -- sodium butyrate -- stromal interaction molecule 1 (STIM1) -- store-operated Ca2+ channel; Molecular biology -- Periodicals; Cytology -- Periodicals; 572.8
• DOI: 10.1042/BSR20110062
• Languages: English
• ISSNs: 0144-8463

Abstract

Abstract : The SOCE (store-operated Ca 2+ entry) pathway plays a key role in both normal cells and cancerous cells. However, its molecular mechanism remains a long-lasting puzzle of Ca 2+ signalling. In this paper, we provide evidence that butyric acid, a dietary fibre-derived short-chain fatty acid, induces apoptosis of colon cancer cells via SOCE signalling networks. We found that sodium butyrate (NaB) induces Ca 2+ release from endoplasmic reticulum, which in turn causes extracellular Ca 2+ influx in HCT-116 cells. The Ca 2+ release and influx are important, because the addition of chelators, EGTA or BAPTA/AM [1, 2-bis-( o -aminophenoxy)ethane- N, N, N ′, N ′-tetra-acetic acid tetrakis(acetoxymethyl ester)] respectively blocked NaB-induced apoptosis. Furthermore, down-regulation of STIM1 (stromal interaction molecule 1) by RNA interference or pharmacological blockade of the SOCC (store-operated Ca 2+ channel) by 2-APB (2-aminoethoxydiphenyl borate) or SKF-96365 inhibited NaB-induced extracellular Ca 2+ influx and apoptosis in HCT-116 cells. Thus we conclude that NaB triggers colon cancer cell apoptosis in an SOCE-dependent manner. This finding provides new insights into how butyric acid suppresses colon carcinogenesis.