Table 1.

Overview of HDAC and its role in cancer.

Tumorigenesis	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, 26–35].
	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].
	HDAC6 inhibition leads to apoptosis [37].
Cell motility or metastasis	HDAC6 overexpression leads to increased cell motility [3, 21, 28, 38].
	HDAC6 inhibition leads to hyperacetylated cortactin and impaired cell motility [15, 17].
	HDAC6 inhibition also leads to its impaired catalytic domain affecting MT dynamism [39].
Transcriptional response	HDAC6 deacetylates Hsp90 and prevents the maturation of glucocorticoid and androgen receptors [40–42].
Translational response	HDAC6 forms a complex with SGs and G3BP1 and eventually induces a reversible translational suppression [43].