Calebin A, a novel component of turmeric, suppresses NF-κB regulated cell survival and inflammatory gene products leading to inhibition of cell growth and chemosensitization.

Amit K Tyagi, Sahdeo Prasad, Muhammed Majeed, Bharat B Aggarwal

Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology 2017;34():171-181

PMID: 28899500

Abstract

BACKGROUND

While the anti-inflammatory and anticancer potential of curcumin, which is derived from turmeric (Curcuma longa), has been studied extensively, very little is known about Calebin A, another novel compound from the same source.

PURPOSE

To determine whether Calebin A exhibits anti-inflammatory and anticancer potential.

METHODS

We examined the anti-inflammatory potential of Calebin A by DNA binding of NF-κB. Anticancer properties of Calebin were determined by MTT and FACS analysis and NF-κB regulated expression of proteins was assessed by western blotting.

RESULTS

Calebin A suppressed NF-κB activation induced by various stimuli. This inhibition of NF-κB activation was mediated through the suppression of direct binding of NF-κB/p65 to the DNA. This inhibitory effect was reversed by a reducing agent, and mutation of the Cys38 of p65 to serine abolished the effect of Calebin A on this binding. Suppression of NF-κB activation by Calebin A resulted in the down-regulation of the expression of proteins involved in tumor cell survival, proliferation, inflammation, and metastasis. Furthermore, Calebin A inhibited proliferation and induced apoptosis in a wide variety of tumor cells, as examined by various assays. It enhanced apoptosis induced by chemotherapeutic agents.

CONCLUSION

Our results demonstrate that Calebin A inhibits NF-κB activation pathway through interaction with p65 and potentiates apoptosis in cancer cells; thus, it has potential in the treatment of cancer. However, further in vivo studies are warranted to define its anti-inflammatory and anticancer potential.

Published by Elsevier GmbH.

Address: Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.; Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA. Electronic address: [email protected].; Sabinsa Corporation, East Windsor, NJ, USA.; Inflammation Research Center, San Diego, CA, USA. Electronic address: [email protected].

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