2013
DOI: 10.1007/s10620-013-2867-7
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The Up-Regulation of Histone Deacetylase 8 Promotes Proliferation and Inhibits Apoptosis in Hepatocellular Carcinoma

Abstract: Our 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.

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Cited by 84 publications
(80 citation statements)
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“…Overexpression of HDAC8 has been reported in a considerable number of different cancer entities [26,34,36,37]. In neuroblastoma, in particular, HDAC8 expression was significantly correlated with further poor prognostic Figure 11 Compensation mechanism after HDAC8 knockdown in RT-112, VM-CUB1, SW-1710, 639-V and UM-UC-3 cells.…”
Section: Discussionmentioning
confidence: 97%
“…Overexpression of HDAC8 has been reported in a considerable number of different cancer entities [26,34,36,37]. In neuroblastoma, in particular, HDAC8 expression was significantly correlated with further poor prognostic Figure 11 Compensation mechanism after HDAC8 knockdown in RT-112, VM-CUB1, SW-1710, 639-V and UM-UC-3 cells.…”
Section: Discussionmentioning
confidence: 97%
“…HDAC8 expression is restricted to specific cell type showing smooth muscle differentiation in normal human tissues (34,36). Although HDAC8 has been shown to promote growth of a number of cancer types (25), (37)(38)(39) and contribute to poor prognosis in childhood neuroblastoma (40), the molecular actions of HDAC8 in cancer remained poorly defined. Although specific HDACs can deacetylate nonhistone proteins (35), emerging data suggest that direct gene repression by HDAC8 might control key pathologic processes (41,42).…”
Section: Discussionmentioning
confidence: 99%
“…The level is similar in cancer and corresponding healthy tissues, with a tendency towards higher expression in cancer tissues [31,43]. Knockdown of HDAC8 by RNA interference (RNAi) inhibits proliferation of human lung, colon, and cervical cancer cell lines (Figure 2), and the upregulation of HDAC8 promotes proliferation and inhibits apoptosis in hepatocellular carcinoma [31,45].…”
Section: Hdac8 and Diseasesmentioning
confidence: 96%
“…A quest for further substrates identified multiple partners, including structural maintenance of chromosomes 3 (SMC3), p53, ERRa, and inv(16) fusion protein [13,14,31,32] (Figure 1; see Glossary). The latest additions are retinoic acid induced 1 (RAI1), zinc finger, RAN-binding domain containing 2 (ZRANB2), nuclear receptor co-activator 3 (NCOA3), thyroid hormone receptor-associated protein 3 (THRAP3), AT-rich interactive domain-containing protein 1A (ARID1A), and cortactin [9,15].…”
Section: Hdac8 Substratesmentioning
confidence: 99%