The relationship between TRAF6 and tumors
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Cancer Cell International Open Access
REVIEW
The relationship between TRAF6 and tumors Jiaoduan Li1,2,3,4,5, Nian Liu1,2,3,4,5, Ling Tang1,2,3,4,5, Bei Yan1,2,3,4,5, Xiang Chen1,2,3,4,5, Jianglin Zhang1,2,3,4,5* and Cong Peng1,2,3,4,5*
Abstract Tumor necrosis factor receptor (TNFR)-related factors (TRAFs) are important linker molecules in the tumor necrosis factor superfamily (TNFSF) and the Toll-like/interleukin-1 receptor (TLR/ILR) superfamily. There are seven members: TRAF1-TRAF7, among those members, tumor necrosis factor receptor-associated factor 6 (TRAF6) is upregulated in various tumors, which has been related to tumorigenesis and development. With the in-depth study of the relationship between TRAF6 and different types of tumors, TRAF6 has oncogenic characteristics involved in tumorigenesis, tumor development, invasion, and metastasis through various signaling pathways, therefore, targeting TRAF6 has provided a novel strategy for tumor treatment. This review summarizes and analyzes the role of TRAF6 in tumorigenesis and tumor development in combination with the current research on TRAF6 and tumors. Keywords: TRAF6, Tumorigenesis, E3 ubiquitin ligase, AP-1, NF-κB Background TRAFs are a class of cytoplasmic adaptor proteins. In mammals, six classical members (TRAF1-TRAF6) and one nonclassical member (TRAF7) are currently known. Classical members are those with a common amino acid segment called a TRAF domain at the carboxy terminus. Nonclassical members do not contain a TRAF homology domain. In 1994, the TRAF family of proteins was discovered as part of the downstream signaling pathway of the tumor necrosis factor superfamily (TNFSF) [1]. Subsequent research showed that the TRAF family of proteins participates in the signaling of the TNFSF and the TLR/ILR receptor superfamily and regulated the activation of signaling pathways such as mitogen-activated protein kinase (MAPK) [2]. In addition, the TRAF family of proteins also participates in cell proliferation, differentiation, survival and apoptosis and engage in immune and inflammatory responses [3]. Among those molecules, TRAF1, TRAF2, TRAF4, TRAF5 and TRAF6 might play carcinogenic roles, whereas TRAF3 acts as a tumor *Correspondence: [email protected]; [email protected] 1 Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China Full list of author information is available at the end of the article
suppressor. TRAF1 and TRAF4 affect on skin and lung carcinoma in mouse model [4–6]. TRAF5 may play a carcinogenic role in colorectal cancer and gastric cancer [7, 8]. TRAF2 promotes tumorigenesis in breast and gastric cancers [9, 10]. However, TRAF3 plays an inhibitory role based on B lymphomas mouse model [11]. TRAF6 has unique receptor binding specificity, which plays an important role in the signaling of the TNF receptor superfamily as well as exerts a specific interaction with members of the IL-1R/TLR superfamily [12]. Studies showed that TRAF6 is overexpressed in various types of tumor, including colon, gastric,
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