Objectives: To investigate the down-regulation mechanism of (bcl-2/adenovirus E1B 19 kDa interacting protein 3 (BNIP3) expression in renal cell carcinoma (RCC).
Methods: RCC cell lines 786-O, ACHN and A498 were treated with different concentrations of histone deacetylase inhibitor TSA. Thereafter, the proliferation of RCC cells was determined with CCK-8 assay, cell apoptosis was observed by flow cytometry, and the expression levels of BNIP3 were determined by Q-PCR and Western blot, and the acetylation status of histone H3 in the promoter of was detected by ChIP.
Results: After the treatment with TSA, the proliferation of the three RCC cell lines was significantly inhibited (<0.05), the early apoptosis of cells obviously increased, and the expression levels of mRNA (<0.05) and protein were up-regulated. The histone H3 in promoter of both 786-O and ACHN was deacetylated, while the histone H3 in promoter of A498 was acetylated.
Conclusions: Histone deacetylation may be the important mechanism of silencing in RCC.
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