The Up-Regulation of Histone Deacetylase 8 Promotes Proliferation and Inhibits Apoptosis in Hepatocellular Carcinoma View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2013-09-28

AUTHORS

Jian Wu, Chengli Du, Zhen Lv, Chaofeng Ding, Jun Cheng, Haiyang Xie, Lin Zhou, Shusen Zheng

ABSTRACT

BackgroundHistone deacetylase 8 (HDAC8), a member of class I HDACs, has been reported to be involved in transcriptional regulation, cell cycle progression, and developmental events, and several studies have shown that HDAC8 plays a critical role in tumorigenesis. However, the expression level and the potential role of HDAC8 in hepatocellular carcinoma (HCC) remain unclear.AimThe purpose of this study was to investigate protein expression of HDAC8 in HCC tissues and the effects of HDAC8 knockdown on the proliferation and apoptosis of liver cancer cells, and to explore the possible mechanisms.MethodsFirst, we used quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR), immunohistochemical staining, and western blot to examine the mRNA and protein expression of HDAC8 in HCC cell lines and tissues. Then, we assessed the correlation between clinicopathological parameters and the protein expression of HDAC8. Furthermore, we employed the interfering RNA method to explore the potential role of HDAC8 in HCC progression in vitro.ResultsOur results showed that expression of HDAC8 was significantly up-regulated both in HCC cell lines and tumor tissues compared to human normal liver cell line LO2 and corresponding non-tumor tissues. Moreover, we found that HDAC8 knockdown could dramatically inhibit HCC cell proliferation and enhance the apoptosis rate in vitro. Western blot revealed that intrinsic apoptotic pathway proteins, including BAX, BAD, and BAK, were elevated after HDAC8 knockdown. The cleavage of caspase-3 and PARP, which are downstream of intrinsic apoptotic pathway, were also enhanced. In addition, suppression of HDAC8 also elevated the expression of p53 and acetylation of p53 at Lys382, whereas the acetylation of p53 at Lys373 did not change.ConclusionsOur study revealed that HDAC8 was overexpressed in HCC. HDAC8 knockdown suppresses tumor growth and enhances apoptosis in HCC via elevating the expression of p53 and acetylation of p53 at Lys382. HDAC8 might serve as a potential therapeutic target in HCC. More... »

PAGES

3545-3553

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s10620-013-2867-7

DOI

http://dx.doi.org/10.1007/s10620-013-2867-7

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1034947324

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/24077923


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74 class I HDACs
75 cleavage
76 clinicopathological parameters
77 correlation
78 critical role
79 cycle progression
80 developmental events
81 effect
82 events
83 expression
84 expression levels
85 expression of HDAC8
86 expression of p53
87 growth
88 hepatocellular carcinoma
89 immunohistochemical staining
90 intrinsic apoptotic pathway
91 intrinsic apoptotic pathway proteins
92 knockdown
93 levels
94 lines
95 liver cancer cells
96 mRNA
97 mechanism
98 members
99 method
100 non-tumor tissues
101 normal liver cell line LO2
102 p53
103 parameters
104 pathway
105 pathway proteins
106 polymerase chain reaction
107 possible mechanism
108 potential role
109 potential therapeutic target
110 progression
111 proliferation
112 protein
113 protein expression
114 purpose
115 quantitative real-time reverse transcription-polymerase chain reaction
116 rate
117 reaction
118 real-time reverse transcription-polymerase chain reaction
119 regulation
120 results
121 reverse transcription-polymerase chain reaction
122 role
123 staining
124 study
125 suppression
126 target
127 therapeutic target
128 tissue
129 transcription-polymerase chain reaction
130 transcriptional regulation
131 tumor growth
132 tumor tissue
133 tumorigenesis
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