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核VANGL2 抑制乳糖分化的作用

Stefany Rubio^1,2, Rut Molinuevo^1,2, Natalia Sanz-Gomez³

¹Institute for the Biology of Stem Cells, University of California, Santa Cruz, CA 95064, USA.

|February 9, 2024

概括

平面细胞极性 (PCP) 蛋白VANGL2移动到核中,调节乳腺细胞的分化. 失去VANGL2功能可以提高STAT5信号的调节,并促进分化.

科学领域:

细胞生物学细胞生物学
发展生物学发展生物学
癌症研究癌症研究

背景情况:

平面细胞极性 (PCP) 蛋白调节组织形态发生和细胞极性.
跨膜PCP蛋白是内细胞化,这表明潜在的细胞内作用.
对于PCP蛋白的核功能,特别是对转录的控制,基本上是未知的.

研究的目的:

研究跨膜PCP蛋白VANGL2.2.的细胞内和潜在的转录作用.
为了确定VANGL2是否影响乳腺分化和相关的信号通路.

主要方法:

在乳腺癌和乳腺细胞系中评估了VANGL2的核定位.
确定了VANGL2的DNA结合能力和核定位信号.
进行了CUT&RUN测试,以绘制VANGL2的基因组结合部位.
Vangl2的淘汰和过度表达研究在细胞系和有机体中进行.

主要成果:

在未分化的乳腺细胞和乳腺癌细胞的核中发现了VANGL2.
Vangl2功能的丧失导致了STAT5信号通路的上调.
VANGL2与DNA结合,包括Stat5a促销物,其敲击对Stat5a,Ccnd1和Csn2.2进行上调.
Vangl2的淘汰诱导了更大的青,早期的分化,以及被野生类型的Vangl2.2拯救的表型.

结论:

像VANGL2这样的跨膜PCP蛋白可以在细胞内发挥作用,调节基因转录.
VANGL2充当转录调节剂,抑制乳腺细胞中的分化程序.
这些发现为通过转录控制协调组织形态发生的PCP蛋白建立了新的范式.

关键词:

这就是VANGL2的意思.乳腺腺腺体乳腺体核定位的核定位

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