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。
更多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.
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