Inflammatory stimuli such as TLR ligands, IL-1&beta, and TNF-&alpha in tumor microenvironment are capable of activating the NF- &kappaB controlled inflammatory responses in cancer cells. The activation of cellular responses by these stimuli are modulated by various molecules including those control ubiquitination and deubiquitination in the NF-&kappa B signaling pathway. The DUB-3 has been identified as a deubiquitinating enzyme that belongs to a family of inducible DUBs. In this study, we found that expression of DUB-3 is increased in lung cancers and associated with poor prognosis, macrophage and inflammatory marker expressions, and cigarette smoking. DUB-3 regulated deubiquitination process in the inflammatory signaling pathways, and controlled inflammation and stemness in cancer cells. In animal studies, overexpression of DUB3 in cancer cell promoter tumor growth. Taken together, there results suggest that DUB3 regulate inflammation and stemness in cancer cells and promoter lung cancer growth.
