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Fig. 8 | Journal of Biomedical Science

Fig. 8

From: Inhibition of histone deacetylase 6 destabilizes ERK phosphorylation and suppresses cancer proliferation via modulation of the tubulin acetylation-GRP78 interaction

Fig. 8

Schematic 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 formation

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