The NFkB signaling pathway in papillomavirus-induced lesions: Friend or foe?

Abstract

Papillomaviruses induce a range of benign and malignant lesions in their hosts, including cervical cancer, that is associated with high-risk human papillomavirus (HPV) types. The nuclear factor kappa-light-chain-enhancer of activated B-cells (NFB) plays a pivotal role in HPV-infected cells, and its expression and activity are modulated by several viral oncoproteins. NFB modulation seems to first facilitate viral persistence and immune evasion, and later to drive tumour progression, but the many conflicting results and the complexity of its signaling networks require great prudence while interpreting the role of NFB in papillomaviral lesions. Accordingly, the pharmacological targeting of the NFB pathway in HPV-induced lesions is a complex and currently unmet challenge. This review deals with recent findings concerning NFB activation in HPVinfected cells, its role in viral persistence, cell transformation and tumour progression, and with current efforts to target this pathway for cancer prevention and therapy.