Zou Junrong, Guo Pei, Lv Nonghua, Huang Deqiang
Research Institute of Digestive Diseases, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Mol Med Rep. 2015 Nov;12(5):6399-404. doi: 10.3892/mmr.2015.4243. Epub 2015 Aug 25.
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.
脂多糖诱导的肿瘤坏死因子-α因子（LITAF）发挥转录因子活性并参与蛋白质质量控制。LITAF的活性高度依赖于从内体/溶酶体到细胞核的正确转运，而某些LITAF突变体则错误定位于细胞质和线粒体等区域，从而导致发育性疾病。此外，先前的研究表明LITAF作为一种肿瘤抑制因子，在某些类型的癌症中经常表达不足。然而，这种现象的机制仍不清楚。本综述总结了LITAF研究的主要进展，并提出LITAF可能作为肿瘤相关炎症中经典激活和替代激活之间平衡的一个开关。因此，就肿瘤微环境而言，LITAF可能是一个有前景的治疗靶点。
