肿瘤坏死因子受体相关因子6促进胃癌细胞自我更新、增殖和迁移。
TRAF6 Promotes Gastric Cancer Cell Self-Renewal, Proliferation, and Migration.
作者信息
Yang Mengting, Jin Meng, Li Kailong, Liu Haifeng, Yang Xiaxia, Zhang Xiaobei, Zhang Bin, Gong Aihua, Bie Qingli
机构信息
Department of Laboratory Medicine, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong, China.
Key Laboratory of Laboratory Medicine of Jiangsu Province, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu, China.
出版信息
Stem Cells Int. 2020 Jul 17;2020:3296192. doi: 10.1155/2020/3296192. eCollection 2020.
Gastric cancer is the third most common type of tumor associated with death. TRAF6 belongs to the tumor necrosis factor receptor-associated factor family and has been demonstrated to be involved in tumor progression in various cancers. However, the exact effect of TRAF6 on gastric cancer stem cells has not been extensively studied. In this study, abnormal expression of TRAF6 was found in gastric cancer tissues. Overexpression of TRAF6 enhanced proliferation and migration, and TRAF6 knockdown reversed this phenomenon in gastric cancer cells. Moreover, TRAF6 may inhibit differentiation and promote stemness and epithelial-mesenchymal transition (EMT). Transcriptome profiles revealed 701 differentially expressed genes in the wild-type group and the TRAF6 knockout group. Potential molecules associated with cell proliferation and migration were identified, including MAPK, FOXO, and IL-17. In conclusion, TRAF6 is a significant factor promoting proliferation and migration in gastric cancer cells and may provide a new target for the accurate treatment of gastric cancer.
胃癌是与死亡相关的第三大常见肿瘤类型。TRAF6属于肿瘤坏死因子受体相关因子家族，已被证明参与多种癌症的肿瘤进展。然而，TRAF6对胃癌干细胞的确切作用尚未得到广泛研究。在本研究中，发现TRAF6在胃癌组织中表达异常。TRAF6的过表达增强了胃癌细胞的增殖和迁移，而TRAF6基因敲低则逆转了这一现象。此外，TRAF6可能抑制分化并促进干性和上皮-间质转化（EMT）。转录组分析揭示了野生型组和TRAF6基因敲除组中有701个差异表达基因。鉴定出了与细胞增殖和迁移相关的潜在分子，包括MAPK、FOXO和IL-17。总之，TRAF6是促进胃癌细胞增殖和迁移的重要因素，可能为胃癌的精准治疗提供新靶点。
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