Abstract 2309: Acetylation of survivin represses transactivation of STAT3 to induce sodium butyrate-induced apoptosis in human mucoepidermoid carcinoma cell lines

Abstract

Abstract Sodium butyrate (NaBu) is one of histone deacetylase inhibitors and possesses anticancer activity. Here, the aim of this study is to determine the molecular mechanism by which NaBu controls apoptosis in MC3 and YD15 human mucoepidermoid carcinoma (MEC) cell lines. NaBu caused growth inhibition and induced apoptosis in both cell lines accompanied by the acetylation of histone proteins H2A and H3. NaBu clearly increased survivin and cleaved caspase 3 evidenced by human apoptosis array and it regulated survivin molecule at a post-transcriptional level. NaBu caused nuclear translocation of survivin protein and increased survivin acetylation in both cell lines. In addition, STAT3 and survivin were co-localized in nucleus by NaBu resulting in the decrease in the expression level of Bcl-XL mRNA which is one of STAT3 downstream molecules. In addition, NaBu induced caspase-dependent apoptosis in human MEC cells. Taken together, these results suggest that NaBu is a potent apoptosis inducer in human MEC cell lines through survivin-STAT3 signaling cascades and these findings provide the basis of its clinical application for the treatment of human MEC. This abstract is supported by SNU Invitation Program for Distinguished Scholar and the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (2014R1A12055874) Citation Format: Sung-Dae Cho. Acetylation of survivin represses transactivation of STAT3 to induce sodium butyrate-induced apoptosis in human mucoepidermoid carcinoma cell lines [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 2309. doi:10.1158/1538-7445.AM2017-2309