DDX17-Mediated Upregulation of CXCL8 Promotes Hepatocellular Carcinoma Progression via Co-activating β-catenin/NF-κB Complex

作者：Hui Liu, Xiaoliang Gao, Wenyao Zhang, Xin Fu, Jing Zhang, Qiangqiang Yuan, Jing Jin, Xinyu Du, Renlong Li, Yan Li, Shuang Yu, Qiujin Zhang, Xianchun Gao, Liang Zhang, Yu‐Wei Ling, Jing Wu, Lin Wang, Jinliang Xing, Fulin Chen, Yongzhan Nie · 发表于：International Journal of Biological Sciences · 年份：2025 · DOI：10.7150/ijbs.104165 · 被引用次数：7 · 研究领域：Chemokine receptors and signaling、Immunotherapy and Immune Responses、Cytokine Signaling Pathways and Interactions

. More interestingly, stimulation with recombinant human CXCL8 augmented the interaction of NF-κB with DDX17/β-catenin and enhanced its autocrine activation by promoting the phosphorylation of IκBα. Furthermore, blocking the association of the DDX17/β-catenin/NF-κB complex with a CXCR1/2 inhibitor markedly abrogated DDX17-mediated HCC proliferation and metastasis. Overall, this study provided new insights into DDX17-mediated pro-inflammatory chemokine activation, which unveiled the association between DDX17 and β-catenin/ NF-κB complex in transactivating the expression of CXCL8. The usage of CXCR1/2 inhibitor to block DDX17-induced CXCL8 signaling activation might be a potential therapeutic approach for HCC treatment.