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CTR9通过JAK2信号通路调控胶质瘤增殖作用的研究
作者:徐阳  张岩松  夏炎  朱帅帅  罗正祥 
单位:南京脑科医院 神经外科, 江苏 南京 210029
关键词:胶质瘤 CTR9 JAK2 信号通路 
分类号:R739.41
出版年·卷·期(页码):2024·52·第十一期(1666-1673)
摘要:

目的: 探讨CTR9(Cln three requiring 9)是否通过JAK2信号通路进而影响胶质瘤细胞的增殖能力。方法: 在公共数据库中分析CTR9的mRNA表达水平以及CTR9相关生存曲线。检测CTR9在胶质瘤组织中的表达,并构建具有稳定沉默或过表达CTR9的U251和T98G细胞系,通过细胞功能试验和Western blotting试验,探讨CTR9对胶质瘤的增殖能力的影响以及具体机制。结果: CTR9在神经胶质瘤中过表达,并与神经胶质瘤患者的生存率呈负相关。结果表明,敲低CTR9抑制了神经胶质瘤细胞的增殖能力,而过表达促进了它们。潜在的分子机制可能涉及CTR9对JAK2/STAT3通路的调节。结论: CTR9可以通过调控JAK2/STAT3信号通路,从而促进胶质瘤的增殖能力。

Objective: To explore the mechanism of CTR9-meidated JAK2 signaling pathway on the proliferation of glioma cells. Methods: We analyzed the expression level of CTR9 mRNA and CTR9-related survival curves in the public database. Then, we detected the expression of CTR9 in glioma tissues and constructed U251 and T98G cell lines with stable silencing or overexpression of CTR9. This study employed cell function tests and Western blotting tests to elucidate the influence and underlying molecular mechanisms of CTR9 on the proliferative capacity of glioma cells. Results: CTR9 was overexpressed in glioma and negatively correlated with the survival of glioma patients. The results indicated that knockdown of CTR9 inhibited the proliferation of glioma cells, whereas overexpression enhanced the process. The underlying molecular mechanism may involve CTR9 regulation of the JAK2/STAT3 pathway. Conclusion: CTR9 can promote the proliferation of glioma by regulating JAK2/STAT3 signaling pathway.

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