HDAC6 expression and its mediated HSF1 activation are essential for tumor growth and maintenance of oncogenic phenotype by promoting anchorage-independent proliferation to transformed cells [3, 26ā35].
CYLD-mediated HDAC6 inhibition leads to delay in the cell cycle and reduced rate of cytokinesis [30, 32].
Cell survival
HDAC6 binds ubiquitinated protein aggregates and this leads to the dissociation of the basal complex, and eventual activation of the aggresome pathway [28, 33, 36].