基因系尾型同源盒基因在腺性膀胱炎发生及癌化的调控新机制研究

Study on the new regulatory mechanism of CDX2 in the occurrence and carcinogenesis of glandular cystitis

目的分析讨论基因系尾型同源盒基因(CDX2)在腺性膀胱炎及其癌化中对调控机制的影响。方法回顾性分析2018年1月至2018年10月本院收治的腺性膀胱炎患者37例,通过CDX2处理,分析MAPK/ERK和JAK2/STAT3两条信号通路对CDX2在腺性膀胱炎的调控及癌化作用。结果通过对患者标本进行CDX2处理72 h后,侵袭穿膜细胞数和迁移穿膜细胞数明显高于处理前,差异具有统计学意义(P<0.05)。通过对患者标本进行CDX2处理72 h后,P-STAT3和P-ERK蛋白明显低于处理前,差异具有统计学意义(P<0.05)。通过对患者标本进行CDX2处理72 h后,STAT3、ERK1和ERK2 mRNA转录水平均出现下降,差异具有统计学意义(P<0.05)。结论MAPK/ERK和JAK2/STAT3两条信号通路存在交互作用,相互影响反转录。而且通过CDX2有效作用,能够激活MAPK/ERK和JAK2/STAT3两条信号通路,抑制腺性膀胱炎的发生以及癌化。

Objective To analyze and discuss the regulatory mechanism of CDX2 gene in glandular cystitis and its carcinogenesis.Methods From January 2018 to October 2018,37 patients with glandular cystitis admitted were retrospectively analyzed.The effects of MAPK/ERK and JAK2/STAT3 signaling pathways on the regulation and carcinogenesis of CDX2 in cystitis glandularis were analyzed by CDX2 treatment.Results After 72 hours of CDX2 treatment,the number of invasive and migrating cells was significantly higher than that before treatment(P<0.05).After 72 hours of CDX2 treatment,P-STAT3 and P-ERK proteins were significantly lower than those before treatment(P<0.05).After 72 hours of CDX2 treatment,the transcription levels of STAT3,ERK1 and ERK2 were all decreased,with statistical significance(P<0.05).Conclusions MAPK/ERK and JAK2/STAT3 signaling pathways interact and interact with each other in reverse transcription.Moreover,CDX2 can activate MAPK/ERK and JAK2/STAT3 signaling pathways and inhibit the occurrence and carcinogenesis of cystitis glandularis.