Romidepsin and bortezomib potently induces apoptosis of NPC cells.

What is it about?

Bortezomib can synergize with romidepsin (class I HDAC inhibitor) to induce apoptosis of cancer cells through an ROS-dependent and ER stress-induced mechanism, independent of HDAC6 inhibition. The data provided a mechanistic rationale to combine the more specific and potent class I HDAC inhibitors with proteasome inhibitors to treat cancers.

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Why is it important?

Synergy between proteasome and histone deacetylase (HDAC) inhibitors resulting in the induction of apoptosis in cancer cells requires inhibition of HDAC6, which normally manages cellular stress by clearing cells of misfolded proteins. Here, a novel HDAC6-independent mechanism involving endoplasmic reticulum (ER) stress-induced apoptosis is described for synergism between proteasome inhibitors and class I HDAC inhibitors, which lack HDAC6 activity, in nasopharyngeal carcinoma. The findings warrant further study of the combined use of proteasome inhibitors with specific and potent class I HDAC inhibitors in the treatment of cancer.

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