Wang Cong, Liu Zhenghuan, Xu Zhihui, Wu Xian, Zhang Dongyang, Zhang Ziqi, Wei Jianqin
Department of Hepatopancreatobiliary Surgery, Affiliated Hospital of Qinghai University, Xining, Qinghai 810001, P.R. China.
Department of Urology, West China School of Medicine, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
Oncol Lett. 2018 Aug;16(2):2071-2077. doi: 10.3892/ol.2018.8896. Epub 2018 Jun 4.
Chemokine ligand 25 (CCL25) and chemokine receptor 9 (CCR9) are important regulators of migration, proliferation and apoptosis in leukocytes and cancer cells. Blocking of the CCR9/CCL25 signal has been demonstrated to be a potential novel cancer therapy. Research into CCR9 and CCL25 has revealed their associated upstream and downstream signaling pathways; CCR9 is regulated by several immunological factors, including NOTCH, interleukin 2, interleukin 4 and retinoic acid. NOTCH in particular, has been revealed to be a crucial upstream regulator of CCR9. Furthermore, proteins including matrix metalloproteinases, P-glycoprotein, Ezrin/Radixin/Moesin and Livin are regulated via phosphatidylinositol-3 kinase/protein kinase B, which are in turn stimulated by CCR9/CCL25. This is a review of the current literature on the functions and signaling pathways of CCR9/CCL25.
趋化因子配体25(CCL25)和趋化因子受体9(CCR9)是白细胞和癌细胞迁移、增殖及凋亡的重要调节因子。已证实阻断CCR9/CCL25信号是一种潜在的新型癌症治疗方法。对CCR9和CCL25的研究揭示了它们相关的上游和下游信号通路;CCR9受多种免疫因子调控,包括NOTCH、白细胞介素2、白细胞介素4和视黄酸。特别是NOTCH,已被揭示为CCR9的关键上游调节因子。此外,包括基质金属蛋白酶、P-糖蛋白、埃兹蛋白/根蛋白/膜突蛋白和生存素在内的蛋白质通过磷脂酰肌醇-3激酶/蛋白激酶B进行调节,而这又受到CCR9/CCL25的刺激。本文综述了有关CCR9/CCL25功能和信号通路的当前文献。