The Role of HDAC6 in Cancer

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].