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人类中介性益生素受体I-tail通过准Ras/MAPK通路促进乳腺瘤发生

Shanwei Shen^1,2, Senthil K Radhakrishnan^1,3, J Chuck Harrell^1,2,3

¹Department of Pathology, Virginia Commonwealth University, Richmond, VA 23298, USA.

|May 7, 2024

概括

益生素受体中间形式的I-尾驱动乳腺癌的生长,通过影响细胞增殖和迁移. 抑制其相关途径,如ERK,显示了新乳腺癌治疗的潜力.

科学领域:

分子生物学分子生物学
在瘤学瘤学.
细胞生物学细胞生物学

背景情况:

益生菌受体 (PRLr) 和其变体与乳腺癌有关.
人类PRLr (hPRLrI) 的中间形式具有独特的13氨基酸I尾.
对hPRLrL和hPRLrI的同时表达对于乳腺上皮质转化至关重要.

研究的目的:

阐明hPRLrI I-tail在益生素受体介导的乳腺瘤发生中的功能作用.
为了研究I尾巴在信号通路和基因表达中的参与.

主要方法:

使用的MCF10AT细胞被改造为表达hPRLrL/hPRLrI或缺乏I尾部的突变细胞 (hPRLrIΔ13).
评估了细胞增殖,独立于定点的生长和迁移.
用于信号通路分析 (Ras/MAPK,PI3K/Akt) 和用于基因表达特征的RNA测序的西斑.

主要成果:

删除I-tail显著降低了细胞增殖,独立于 anchorage的生长,并减弱了细胞迁移.
发现I-tail参与Ras/MAPK信号传输,特别影响ERK活动,并影响hPRLrI的稳定性.
RNA测序揭示了I尾部被移除后由益生菌诱导的差异性基因表达;ERK1/2抑制降低了增殖和殖民地形成.

结论:

hPRLrI I-tail 是乳腺癌发生的一个关键因素,促进了增殖,生长和迁移.
针对I-tail或其相关的信号通路,如ERK,为乳腺癌提供了潜在的治疗策略.
对I-tail机制的进一步研究可能会导致新的乳腺癌治疗方法.

关键词:

拉斯/马普克 (Ras/MAPK) 是一种乳腺癌乳腺癌乳腺癌益生菌蛋白是一种益生菌素.益生菌受体的受体是益生菌受体.

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