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.

中文翻译：

---

TRAF6促进胃癌细胞的自我更新，增殖和迁移。

胃癌是与死亡有关的第三大常见肿瘤。TRAF6属于肿瘤坏死因子受体相关因子家族，并已证明与多种癌症的肿瘤进展有关。然而，尚未广泛研究TRAF6对胃癌干细胞的确切作用。在这项研究中，在胃癌组织中发现了TRAF6的异常表达。TRAF6的过表达增强了增殖和迁移，而TRAF6敲低逆转了胃癌细胞中的这种现象。此外，TRAF6可能抑制分化并促进茎干和上皮-间质转化（EMT）。转录组图谱显示野生型组和TRAF6基因敲除组中701个差异表达的基因。确定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，并可能为准确治疗胃癌提供新的靶点。