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TMEM97/Sigma 2受体增加雌激素受体α活动,促进乳腺癌细胞生长

Yuanqin Zhang¹, Xiangwei Fang¹, Jiuhui Wang¹

¹Department of Medical Microbiology, Immunobiology and Cell Biology, Southern Illinois University School of Medicine and Simmons Cancer Institute, Springfield, IL 62702, USA.

|December 9, 2023

概括

TMEM97/sigma 2受体在ER阳性乳腺瘤中高度表达,驱动瘤生长和他莫西芬耐药性. 准TMEM97可能为乳腺癌患者提供新的治疗策略.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
内分泌学在内分泌学.

背景情况:

异常的雌激素受体 (ER) 信号驱动乳腺瘤的生长.
参与乳腺癌发生的西格玛2受体的分子身份是难以捉摸的,直到TMEM97被确定.
TMEM97/sigma 2受体表达与ER阳性乳腺瘤有关.

研究的目的:

研究TMEM97/sigma 2受体在ER阳性乳腺癌中的作用.
为了确定TMEM97表达和临床参数之间的相关性.
阐明 TMEM97 影响乳腺癌细胞生长和治疗反应的分子机制.

主要方法:

对乳腺瘤中TMEM97表达的分析以及与ER,PR和HER2状态的相关性.
在各种条件下评估TMEM97对乳腺癌细胞增殖和存活率的影响.
研究TMEM97对ERα转录活性,mTOR/S6K1信号传递和他莫西芬敏感性的影响.
使用基因淘汰和药理抑制 (mTOR 抑制剂).

主要成果:

在ER阳性乳腺瘤中,TMEM97的表达很高,与ER/PR状态和患者存活率降低相关.
增加TMEM97的表达增强了乳腺癌细胞的生长,促进对他莫西芬的耐药性,并支持在雌激素贫乏条件下的生长.
TMEM97对ERα转录活性进行上调,并刺激mTOR/S6K1信号通路.
mTOR 抑制阻断了 TMEM97 诱导的 ERα 激活和他莫西芬耐药性; TMEM97 敲击使细胞对他莫西芬敏感.

结论:

TMEM97/sigma 2受体是乳腺瘤细胞中ERα活性的一种新型调节器.
TMEM97表达是ER阳性乳腺癌的显著预后标志物.
准TMEM97或其下游信号通路 (mTOR) 可能是克服乳腺癌中他莫西芬耐药性的治疗策略.

关键词:

这就是S6K1的原因.在TEMEM97中,TEMEM97是TEMEM97中的一个.雌激素受体α 是一种雌激素受体.在mTOROR中使用mTOR.西格玛受体的受体泰莫西芬 (Tamoxifen) 是一种

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