Lipopolysaccharide-induced tumor necrosis factor-α factor enhances inflammation and is associated with cancer (Review).

Lipopolysaccharide-induced tumor necrosis factor-α factor (LITAF) exerts transcription factor activity and is involved in protein quality control. LITAF activity is highly dependent on correct translocation from the endosome/lysosome to the nucleus, while certain LITAF mutants mislocalize to areas, such as the cytosol and mitochondria, resulting in developmental diseases. In addition, previous studies have proposed that LITAF functions as a tumor suppressor and is frequently under‑represented in certain types of cancer. However, the mechanism of this phenomenon remains unclear. The present review summarizes the major advances in LITAF studies, and proposes that LITAF may serve as a switch in the balance between classical and alternative activation in tumor associated‑inflammation. Thus, LITAF may be a promising therapeutic target with regard to the tumor microenvironment.