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Evaluating the risk category of gastrointestinal stromal tumors (GISTs) is crucial for predicting prognosis and choosing treatment strategies, and tumor metastasis usually represent poor prognosis. Tumor necrosis factor-alpha-induced protein 8-like 2 (TIPE2) is a novel described tumor suppressor. In the present study, TIPE2 expression was detected using a total of 96 human GIST specimens by immunohistochemistry. The effect of TIPE2 on proliferation and invasiveness of GIST cells and its related mechanisms were explored in vitro. It was found that TIPE2 expression was gradually decreased in accordance with GIST risk grades and negatively associated with tumor size, mitotic count and risk category. Moreover, TIPE2 was identified as a biomarker for evaluating the risk grade of GIST. TIPE2 markedly suppressed the viability, colony formation, migration and invasion of GIST cells. Furthermore, TIPE2 induced apoptosis and suppressed MMP-9 expression of GIST cells by targeting Rac1. In conclusion, these results indicate that TIPE2 plays a pivotal role in the progression of GIST. TIPE2 serves as a promising biomarker for evaluating GIST risk grade and a potential target for treatment of GIST.

Background Tumor necrosis factor (TNF)-alpha-induced protein 8-like 2 (TIPE2 or TNFAIP8L2) is a newly described negative immune regulator and is closely associated with various tumors. However, the expression and roles of TIPE2 in PTC is unknown. Results In the present study, TIPE2 upregulation in PTC tissues was found to be negatively associated with tumor size, capsule infiltration, peripheral infiltration and tumor T stage, which could be used to predict tumor invasiveness. TIPE2 overexpression significantly suppressed the viability, proliferation, migration and invasion of PTC cells. Moreover, TIPE2 suppressed tumor invasiveness by inhibiting Rac1, leading to decreased expression of uPA and MMP9. Conclusions These results indicate that TIPE2 is a potential biomarker for predicting tumor aggressiveness and suppresses tumor invasiveness in a Rac1-dependent manner. Electronic supplementary material The online version of this article (10.1186/s13578-018-0247-x) contains supplementary material, which is available to authorized users.