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在 stromal 纤维细胞中的 Pten 抑制了乳腺上皮瘤
Anthony J Trimboli1, Carmen Z Cantemir-Stone, Fu Li
1Department of Molecular Genetics, College of Biological Sciences, The Ohio State University, Columbus, Ohio 43210, USA.
Nature
|October 23, 2009
概括
乳腺流体中Pten的损失通过破坏瘤微环境来加速表皮瘤的生长. 向 stromal 纤维细胞中的 Pten-Ets2 信号轴可以抑制瘤进展,并提供一种潜在的治疗策略.
科学领域:
- 在瘤学瘤学.
- 癌症生物学 癌症生物学
- 细胞信号传输 细胞信号传输
背景情况:
- 瘤侧膜在上皮瘤恶性瘤中起着至关重要的作用,但细胞间信号传输仍然不太了解.
- 了解体贡献对于开发有效的癌症疗法至关重要.
研究的目的:
- 为了研究酸酶和素同类素 (Pten) 在乳腺 stromal 纤维细胞中的作用.
- 为了阐明涉及到Pten介导的瘤抑制中的信号通路.
主要方法:
- 在小鼠乳腺 stromal 纤维细胞中 Pten 的遗传失活化.
- 对瘤发病,进展和恶性转变的分析.
- 评估细胞外矩阵重塑,免疫细胞透和血管生成.
- 研究了Ets2转录因子的作用.
- 全球基因表达造型乳腺 stromal 细胞.
主要成果:
- 在流体纤维细胞中Pten无活化加速了乳腺上皮瘤发生.
- 这种加速与ECM重塑,免疫细胞透和血管生成增加有关.
- 失去Pten会增加Ets2的表达,酸化和促进体的招募.
- 在Pten缺陷层中Ets2无活化改善了瘤微环境的破坏,并减少了瘤的生长.
- 在肌肉细胞中发现了一种特定于Pten的基因表达特征,并在人类乳腺癌肌肉细胞中发现了这种特征.
结论:
- stromal 纤维细胞中的 Pten-Ets2 信号轴作为乳腺上皮瘤的关键抑制剂.
- 准这种特定于胸膜的途径可能为乳腺癌提供新的治疗策略.
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