We have located links that may give you full text access.
ENGLISH ABSTRACT
JOURNAL ARTICLE
[Histone Deacetylation Down-regulates the Expression of BNIP3 in Renal Cell Carcinoma].
Sichuan da Xue Xue Bao. Yi Xue Ban = Journal of Sichuan University. Medical Science Edition 2017 May
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.
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.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices 
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app