IκB‑α: At the crossroad between oncogenic and tumor‑suppressive signals (Review)
- Alessandro Morotti
- Sabrina Crivellaro
- Cristina Panuzzo
- Giovanna Carrà
- Angelo Guerrasio
- Giuseppe Saglio
Published online on: December 6, 2016
Copyright: © Morotti et al.
This is an open access article distributed under the terms of Creative Commons Attribution License.
Nuclear factor κB (NF‑κB) is an essential component of tumorigenesis and resistance to cancer treatments. NFKB inhibitor α (IκB‑α) acts as a negative regulator of the classical NF‑κB pathway through its ability to maintain the presence of NF‑κB in the cytoplasm. However, IκB‑α is also able to form a complex with tumor protein p53, promoting its inactivation. Recently, we demonstrated that IκB‑α is able to mediate p53 nuclear exclusion and inactivation in chronic myeloid leukemia, indicating that IκB‑α can modulate either oncogenic or tumor‑suppressive functions, with important implications for cancer treatment. The present review describes the role of IκB‑α in cancer pathogenesis, with particular attention to hematological cancers, and highlights the involvement of IκB‑α in the regulation of p53 tumor‑suppressive functions.