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Table 5 Mechanisms of HDACis in GBM

From: The application of histone deacetylases inhibitors in glioblastoma

alterations

affected part

agents

p21Waf1/Cip1, p27↑

cell cycle arrest

SAHA [151], I-BET151 [164], TSA [165], NaB [166], PB [167], FK228 [168], DATS [169], PXD-101 [170], NBM-HD-3 [171], Scriptaid [172], MS-275 [173]

DR5, TNFα, p53, Bad, Bax, Bim, chop, Puma, m-calpian↑

proapoptotic genes

SAHA [151], TSA [166], NaB [166], VPA [174], FK228 [152], DATS [169], PXD-101 [170], DWP0016 [175]

vasculogenic mimicry, VEGF, EGFR↓

angiogenesis

SAHA , MS-275, MC1568, TSA [176], NaB [177], DATS [169], LBH589 [178]

Bcl2, Bcl-XL↓

antiapoptotic genes

VPA [174], PB [167], FK228 [168], DATS [169]

EZH2, MMP-2↓

invasion

SAHA [179], VPA [174], FK228 [168], W2 [180]

p-PTEN/p-AKT, pFAK/p-STAT3↓

pathways

TSA [181], DATS [169], NBM-HD-3 [171], W2 [180]

CDK2, CDK4, CDK6, cyclins D1, cyclins D2↓

progrowth genes

SAHA [151], TSA [165]

caspase 8, caspase 9, caspase 3

apoptotic cascade activation

SAHA [182], DATS [169]

HOTAIR↓

tumor promoting lncRNA

I-BET151 [183]

Ras, c-myc↓

oncogenes

Scriptaid [172], DATS [169]

CD133, Bmi1↓

GSCs markers

SAHA [182]

  1. ‘↑’ or ‘↓’, represent the up-regulated or down-regulated trend of gene expression, respectively.