HDAC7 levels are increased in RAS-transformed cells, in which this protein was required not only for proliferation and cancer stem-like cell growth, but also for invasive features.
Recently, we identified that histone deacetylases HDAC1 and HDAC7 are necessary to maintain cancer stem cells (CSCs) in both breast and ovarian tumors.
We conclude that HDAC7 has a potent anti-oncogenic effect on specific B-cell malignancies, indicating that its deregulation may contribute to the pathogenesis of the disease.
We identified HDAC1 and HDAC7 as novel targets of miR-34a in breast cancer, and further uncovered that deacetylation of HSP70 K246 by HDAC1 and HDAC7 promotes cancer cell survival and therapy resistance by inhibiting autophagic cell death.
In particular, histone deacetylase 7 (HDAC7), a member of class IIa HDACs, is crucial to maintain cell homeostasis, and HDAC7 has emerged as a new target for cancer therapy.