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BUB1诱导AKT/mTOR通路活动,促进EMT诱导在人类小细胞肺癌中

Moufeng Wang^1,2,3, Lijie You³, Zhixiong Su³

¹Department of Oncology, The First Affiliated Hospital of Fujian Medical University, No. 20 Chazhong Road, Fuzhou, 350005, Fujian, China.

Scientific reports

|September 4, 2024

概括

在小细胞肺癌 (SCLC) 中,BUB1 (由Benzimidazole 1) 抑制的布丁促进了攻击性行为. 它的抑制影响了上皮细胞-介质细胞过渡和AKT/mTOR信号传递,为SCLC提供了潜在的治疗点.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

小细胞肺癌 (SCLC) 是一种侵略性的恶性瘤.
BUB1 (由本齐米达1无抑制的布丁) 涉及各种癌症.
在SCLC病变发生过程中BUB1的作用需要进一步阐明.

研究的目的:

研究BUB1在SCLC中的功能意义.
确定BUB1在SCLC进展中的作用背后的分子机制.
评估BUB1对细胞增殖,迁移,入侵和上皮-介质细胞过渡 (EMT) 的影响.

主要方法:

基因表达综合 (GEO) 数据库分析和免疫组织化学染色以评估BUB1的表达.
细胞增殖 (CCK-8),迁移 (3D伤口愈合) 和入侵 (Transwell) 试验.
西方免疫注射用于分析EMT标记物和AKT/mTOR信号通路组件.

主要成果:

与正常的支气管细胞相比,BUB1在SCLC细胞系中显著上调.
过度表达BUB1促进SCLC细胞的增殖,迁移和入侵.
通过对E-cadherin进行上调和对N-cadherin,Vimentin,ZEB-1和Snail进行下调,BUB1沉默可以逆转EMT.
丢失BUB1减少了AKT和mTOR的酸化,这表明AKT/mTOR通路的抑制.

结论:

在SCLC中,BUB1充当瘤促进剂.
通过激活AKT/mTOR信号,BUB1可以调节SCLC中的EMT.
向BUB1可能是SCLC的新治疗策略.

关键词:

在 AKT/mTOR 中使用.一个BUB1一个BUB1 在EMT中,EMT是EMT.小细胞肺癌是一种小细胞肺癌.

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