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HDAC inhibitor, TSA, downregulates Myc transcription in human cervical cancer cell lines
Author(s) -
Li Hui,
Li Xiaoling,
Liu Xuefeng,
Wu Xinxing
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.699.4
Subject(s) - trichostatin a , hela , histone deacetylase inhibitor , histone deacetylase , chromatin , cancer research , microbiology and biotechnology , chemistry , cell culture , downregulation and upregulation , histone , transcription factor , transcription (linguistics) , promoter , cell , biology , gene expression , gene , biochemistry , linguistics , philosophy , genetics
Histone deacetylase (HDAC) inhibitors have shown promise in clinical cancer therapy and to induce p21 expression in a p53‐independent manner via increased acetylation of the chromatin at the Sp1 sites in the p21 promoter region. Our previous study has shown that Trichostatin A (TSA), a HDAC inhibitor, induces p21 through downregulation of Myc expression and release of Myc bound from the p21 promoter in HeLa cells. However, the mechanism of how TSA downregulates Myc remains unclear. In this study, we treated two human cervical cancer cell lines, HeLa and SiHa, with TSA, confirming that TSA decreased Myc protein with Western blot. The decreased level of Myc might be due to a decreased stability of Myc protein or downregulated transcription of Myc in TSA treated cells. Our results from both regular RT‐PCR and real time RT‐PCR demonstrated a significant decrease of Myc mRNA in TSA treated cells compared to that in untreated cells. Thus, TSA treatment downregulates Myc expression at the transcriptional level in human cervical cancer cell lines. The results provide the possibility that TSA may alter chromatins at the Myc promoter via direct or indirect modifications. Chromatin changes at the Myc promoter in TSA treated cells are being investigated. This work was supported by grant from the National Natural Science Foundation of China (No. 30500465, No. 30810103052) .