Sourav Banerjee, PhD, UC San Diego School of Medicine postdoctoral scholar, cautions that curcumin alone may not be the answer.

“In general, curcumin is expelled from the body quite fast,” said Banerjee. “For curcumin to be an effective drug, it needs to be modified to enter the blood stream and stay in the body long enough to target the cancer. Owing to various chemical drawbacks, curcumin on its own may not be sufficient to completely reverse cancer in human patients.”

Banerjee and colleagues report that curcumin binds to and inhibits DYRK2 leading to the impediment of the proteasome. There are several proteasome inhibitor drugs used in the treatment of multiple myeloma currently (ixazomib, bortezomib, carfilzomib). 

“Our results reveal an unexpected role of curcumin in DYRK2-proteasome inhibition and provide a proof-of-concept that pharmacological manipulation of proteasome regulators may offer new opportunities for hard-to-treat triple-negative breast cancer and multiple myeloma treatment,” said Dixon, who was co-senior author with Zhejiang University’s Xing Guo, PhD, on the paper. “Our primary focus is to develop a chemical compound that can target DYRK2 in patients with these cancers.”

When used in combination with the multiple myeloma drug carfilzomib, curcumin induced a much higher cancer cell death while normal non-cancerous cells were less affected. This suggest that targeting proteasome regulators (such as DYRK2) in combination with proteasome inhibitors may be a promising approach of anticancer therapy with less side-effects but further work is needed, said Banerjee.