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• W2794135090 abstract "Abstract Objectives Histone deacetylases ( HDAC s) are commonly dysregulated in cancer and represent promising therapeutic targets. However, global HDAC inhibitors have shown limited efficacy in the treatment of solid tumours, including hepatocellular carcinoma ( HCC ). In this study, we investigated the therapeutic effect of selectively inhibiting HDAC 1 and 2 in HCC . Methods HDAC 1 inhibitor Tacedinaline ( CI 994), HDAC 2 inhibitor Santacruzamate A ( CAY 10683), HDAC 1/2 common inhibitor Romidepsin ( FK 228) and global HDAC inhibitor Vorinostat ( SAHA ) were used to treat HCC cells. Cell cycle, apoptosis and the protein levels of CDK s and CDKN s were performed to evaluate HCC cell growth. Inhibition of HDAC 1/2 by RNA i was further investigated. Results Combined inhibition of HDAC 1/2 led to HCC cell morphology changes, growth inhibition, cell cycle blockage and apoptosis in vitro and suppressed the growth of subcutaneous HCC xenograft tumours in vivo. p21 Waf1/Cip1 and p19 INK 4d , which play roles in cell cycle blockage and apoptosis induction, were upregulated. Inhibition of HDAC 1/2 by si RNA further demonstrated that HDAC 1 and 2 cooperate in blocking the cell cycle and inducing apoptosis via p19 INK 4d and p21 Waf1/Cip1 upregulation. Finally, H3K18, H3K56 and H4K12 in the p19 INK 4d and p21 Waf1/Cip1 promoter regions were found to be targets of HDAC 1/2. Conclusions Pharmacological or transcriptional inhibition of HDAC 1/2 increases p19 INK 4d and p21 Waf1/Cip1 expression, decreases CDK expression and arrests HCC growth. These results indicated a potential pharmacological mechanism of selective HDAC 1/2 inhibitors in HCC therapy." @default.
• W2794135090 created "2018-03-29" @default.
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• W2794135090 date "2018-02-27" @default.
• W2794135090 modified "2023-10-18" @default.
• W2794135090 title "Pharmacological or transcriptional inhibition of both HDAC1 and 2 leads to cell cycle blockage and apoptosis via p21^Waf1/Cip1 and p19^INK4d upregulation in hepatocellular carcinoma" @default.
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• W2794135090 doi "https://doi.org/10.1111/cpr.12447" @default.
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