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CDCA7-regulated inflammatory mechanism through TLR4/NF-κB signaling pathway in stomach adenocarcinoma
Biofactors ( IF 5.0 ) Pub Date : 2021-08-02 , DOI: 10.1002/biof.1773
Yu Guo 1 , Kaimei Zhou 1 , Xiang Zhuang 1 , Junjie Li 1 , Xianglin Shen 1
Affiliation  

To investigate the role of cell division cycle associated 7 (CDCA7) in stomach carcinoma, detect whether CDCA7 knockdown could regulate the development of stomach carcinoma, and further observe the relationship between CDCA7 and inflammation through TLR4/NF-κB signaling pathway in stomach adenocarcinoma (STAD) in vitro and in vivo. TIMER2.0, Kaplan–Meier plotter, Target Gene, and GEPIA systems were used to predict the potential function of CDCA7. Western blot and immunohistochemistry was used to analyze the expression of CDCA7 at different tissue or cell lines. The proliferation, development, inflammation, and apoptosis of STAD in vitro and in vivo were observed by using CDCA7 knockdown lentivirus through TLR4 suppression by its inhibitor. Bioinformatics analysis of CDCA7 with inflammation and western blot of CDCA7 with target protein of immune-associated cells were observed by using CDCA7 knockdown lentivirus in vivo. Finally, the prognosis and associated of CDCA7 in some gene mutations of STAD was observed by Target Gene system. CDCA7 expression in STAD tumor tissue was higher than the normal. The CDCA7 expression in tumor or MGC803 cells was increased. Furthermore, CDCA7 knockdown lentivirus could inhibit STAD development in vitro and in vivo through weakening tumor cells proliferation, reducing tumor volume and biomarker levels, and then increasing apoptotic level. CDCA7 is possibly able to regulate inflammation in STAD through TLR4/NF-κB signaling pathway. Furthermore, CDCA7 may be related with mast cells and the upstream target factor of TLR4/NF-κB signaling pathway in inflammation. These results may provide a new strategy to stomach carcinoma development by regulating inflammation.

中文翻译:

CDCA7通过TLR4/NF-κB信号通路调控胃腺癌炎症机制

探讨细胞分裂周期相关7(CDCA7)在胃癌中的作用,检测CDCA7敲低是否可以调控胃癌的发展,并通过TLR4/NF-κB信号通路进一步观察CDCA7与胃腺癌炎症的关系。 STAD) 体外和体内。TIMER2.0、Kaplan-Meier 绘图仪、Target Gene 和 GEPIA 系统用于预测 CDCA7 的潜在功能。Western印迹和免疫组织化学用于分析CDCA7在不同组织或细胞系中的表达。使用CDCA7敲低慢病毒,通过其抑制剂抑制TLR4,观察STAD在体外和体内的增殖、发展、炎症和凋亡。使用CDCA7敲低慢病毒在体内观察CDCA7与炎症的生物信息学分析和CDCA7与免疫相关细胞靶蛋白的蛋白质印迹。最后通过Target Gene系统观察CDCA7在STAD部分基因突变中的预后及相关性。STAD肿瘤组织中CDCA7表达高于正常。肿瘤或MGC803细胞中CDCA7的表达增加。此外,CDCA7 敲低慢病毒可通过减弱肿瘤细胞增殖、减少肿瘤体积和生物标志物水平,然后增加细胞凋亡水平,在体外和体内抑制 STAD 的发展。CDCA7 可能能够通过 TLR4/NF-κB 信号通路调节 STAD 中的炎症。此外,CDCA7可能与肥大细胞和炎症中TLR4/NF-κB信号通路的上游靶因子有关。这些结果可能通过调节炎症为胃癌发展提供新的策略。
更新日期:2021-08-02
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