Fig. 8From: Inhibition of histone deacetylase 6 destabilizes ERK phosphorylation and suppresses cancer proliferation via modulation of the tubulin acetylation-GRP78 interactionSchematic model of HDAC6 regulating lung cancer cell growth. HDAC6 functions to deacetylate tubulin, on which the p-ERK/GRP78 complex preferentially localizes, which is required for stabilizing ERK activity. Suppression of HDAC6 by TSA and siHDAC6 caused hyperacetylated tubulin and consequently p-ERK/GRP78 dissociation from microtubules. ERK activity is destabilized and decreased, leading to suppression of cancer cell proliferation and spheroid formationBack to article page