Abstract: Objective 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 BNIP3 was detected by ChIP. Results After the treatment with TSA，the proliferation of the three RCC cell lines was significantly inhibited (PBNIP3 mRNA (PBNIP3 promoter of both 786-O and ACHN was deacetylated，while the histone H3 in BNIP3 promoter of A498 was acetylated. Conclusion Histone deacetylation may be the important mechanism of BNIP3 silencing in RCC.