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Nuclear factor- κ B (NF- κ B) has a vital role in cell survival. Inhibition of NF- κ B has been proven to be an efficient therapeutic pathway for various cancers. Activation of NF- κ B is mainly through serine residues' phosphorylation of inhibitor of  κ B α  (I κ B α ) by IKK complex. Phosphorylation at tyrosine 42 is an alternative pathway in regulation of I κ B α  and NF- κ B signaling, though little is known about the underlying mechanism. Here we identified regulator of calcineurin 1 (RCAN1) as a novel endogenous inhibitor of NF- κ B signaling pathway. RCAN1 can interact with I κ B α  and affect the phosphorylation of I κ B α  at tyrosine 42. Overexpression of RCAN1 by adenovirus reduced cell viability in lymphoma Raji cells and restrained the growth of lymphoma transplants in mice. We further found that N terminus 1–103aa of RCAN1 is sufficient to inhibit NF- κ B and reduce cell viability of lymphoma cells. Our study implicated a novel therapeutic approach for lymphoma by RCAN1 through inhibition of NF- κ B signaling.

The RCAN1 inhibits NF-κB and suppresses lymphoma growth in mice