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  • Open Access

    ARTICLE

    Structure, function, and mechanism of the TNFAIP8 (TIPE) family of proteins in cancer and inflammation

    ZIPENG LIN1,#, CHUXI TANG1,#, LE KANG2, GUANXI LAI1, SHIWEN LIU1, YIXIANG WU1, HUIQUN TIAN3,*, SONG LIU1,4,5,*

    BIOCELL, Vol.47, No.10, pp. 2217-2232, 2023, DOI:10.32604/biocell.2023.030233 - 08 November 2023

    Abstract The multiple roles of the tumor necrosis factor (TNF)-α-inducible protein 8 (TNFAIP8), also named TIPE family of proteins have been shown in tumor and inflammation progression and regulation of cellular autophagy and apoptosis. In this review, we found that the TIPE family showed highly homologous sequences and conserved functional domains, such as the death effector domain (DED)-like domain but displayed different roles and mechanisms in different biological activities. For example, while TIPE is primarily associated with tumor progression and antitumor drug resistance, TIPE1 suppresses tumor progression in most instances. TIPE2 has multiple roles in tumor More > Graphic Abstract

    Structure, function, and mechanism of the TNFAIP8 (TIPE) family of proteins in cancer and inflammation

  • Open Access

    ARTICLE

    Tumor Necrosis Factor (TNF)-α-Induced Protein 8-like-2 (TIPE2) Inhibits Proliferation and Tumorigenesis in Breast Cancer Cells

    Ke Wang, Yu Ren, Yang Liu, Jian Zhang, Jian-jun He

    Oncology Research, Vol.25, No.1, pp. 55-63, 2017, DOI:10.3727/096504016X14719078133320

    Abstract Tumor necrosis factor-a (TNF-a)-induced protein 8-like-2 (TNFAIP8L2 or TIPE2), a member of the tumor necrosis TNFAIP8 family, was found to be involved in the development and progression of several tumors. However, to date, the role of TIPE2 in breast cancer is still unclear. Thus, the aim of this study is to explore the role of TIPE2 in breast cancer. Our results indicated that TIPE2 expression was significantly decreased in human breast cancer tissue and cell lines. Overexpression of TIPE2 inhibited the proliferation in vitro and tumor xenograft growth in vivo. TIPE2 also inhibited the migration/invasion More >

  • Open Access

    ARTICLE

    TIPE2 Overexpression Suppresses the Proliferation, Migration, and Invasion in Prostate Cancer Cells by Inhibiting PI3K/Akt Signaling Pathway

    Qiang Lu, Zhe Liu, Zhuo Li, Jia Chen, Zhi Liao, Wan-rui Wu, Yuan-wei Li

    Oncology Research, Vol.24, No.5, pp. 305-313, 2016, DOI:10.3727/096504016X14666990347437

    Abstract Tumor necrosis factor-a (TNF-a)-induced protein 8-like 2 (TNFAIP8L2, TIPE2) is involved in the invasion and metastasis of human tumors. However, the functional role of TIPE2 in prostate cancer remains unclear. In the present study, we explored the role of TIPE2 in prostate cancer and cancer progression including the molecular mechanism that drives TIPE2-mediated oncogenesis. Our results showed that TIPE2 was lowly expressed in human prostate cancer tissues and cell lines. In addition, restored TIPE2 obviously inhibits proliferation in prostate cancer cells. TIPE2 overexpression also suppresses the epithelial–mesenchymal transition (EMT) process and migration/invasion in prostate cancer More >

  • Open Access

    ARTICLE

    TIPE2 Inhibits Hypoxia-Induced Wnt/β-Catenin Pathway Activation and EMT in Glioma Cells

    Zhi-jun Liu*1, Hong-lin Liu*1, Hai-cun Zhou, Gui-cong Wang*

    Oncology Research, Vol.24, No.4, pp. 255-261, 2016, DOI:10.3727/096504016X14666990347356

    Abstract Hypoxia-induced epithelial-to-mesenchymal transition (EMT) could facilitate tumor progression. TIPE2, the tumor necrosis factor-α (TNF-α)-induced protein 8-like 2 (also known as TNFAIP8L2), is a member of the TNF-α-induced protein 8 (TNFAIP8, TIPE) family and has been involved in the development and progression of several tumors. However, the effects of TIPE2 on the EMT process in glioma cells and the underlying mechanisms of these effects have not been previously reported. In our study, we assessed the roles of TIPE2 in the EMT process in glioma cells in response to hypoxia. Our results indicated that TIPE2 expression was More >

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