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Updated: Feb 28, 2026
Assays for Validating Histone Acetyltransferase Inhibitors
Published on: August 6, 2020
[Histone Deacetylation Down-regulates the Expression of BNIP3 in Renal Cell Carcinoma]
Jian-Bang Liu1,2, Hai-Zhou Wang1,2, Zhen-Hua Liu1,2
1Department of Urology, West China Hospital, Sichuan University, Chengdu 610041, China.
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 BNIP3 was detected by ChIP.
Results:
After the treatment with TSA, the proliferation of the three RCC cell lines was significantly inhibited (P<0.05), the early apoptosis of cells obviously increased, and the expression levels of BNIP3 mRNA (P<0.05) and protein were up-regulated. The histone H3 in BNIP3 promoter of both 786-O and ACHN was deacetylated, while the histone H3 in BNIP3 promoter of A498 was acetylated.
Conclusions:
Histone deacetylation may be the important mechanism of BNIP3 silencing in RCC.
Insights
Histone deacetylation may silence bcl-2/adenovirus E1B 19 kDa interacting protein 3 (BNIP3) in renal cell carcinoma (RCC). TSA treatment inhibited RCC cell proliferation and increased apoptosis, up-regulating BNIP3 expression.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Renal cell carcinoma (RCC) is a significant health concern.
- The role of BNIP3 (bcl-2/adenovirus E1B 19 kDa interacting protein 3) in RCC is not fully understood.
- Investigating gene expression regulation mechanisms in RCC is crucial for therapeutic development.
Purpose of the Study:
- To elucidate the mechanism of down-regulation of BNIP3 expression in RCC.
- To examine the effect of histone deacetylase inhibition on RCC cell behavior and BNIP3 expression.
Main Methods:
- Utilized RCC cell lines (786-O, ACHN, A498) treated with Trichostatin A (TSA), a histone deacetylase inhibitor.
- Assessed cell proliferation using CCK-8 assay and apoptosis via flow cytometry.
- Quantified BNIP3 mRNA and protein levels by Q-PCR and Western blot, respectively.
- Determined histone H3 acetylation status at the BNIP3 promoter using ChIP assay.
Main Results:
- TSA treatment significantly inhibited proliferation and increased early apoptosis in all tested RCC cell lines (P<0.05).
- BNIP3 mRNA and protein expression levels were significantly up-regulated post-TSA treatment (P<0.05).
- Histone H3 in the BNIP3 promoter was deacetylated in 786-O and ACHN cells, but acetylated in A498 cells.
Conclusions:
- Histone deacetylation appears to be a key mechanism contributing to BNIP3 silencing in RCC.
- Targeting histone deacetylases may represent a potential therapeutic strategy for RCC by modulating BNIP3 expression.
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