Fascin1 is known to participate in the migration of cancer cells by binding to actin filaments. Recent studies evidenced that fascin1 also modulates processes such as the tumorigenesis and maintenance of pluripotency genes in cancer stem cells. However, the function of fascin1 in embryonic stem cells remains unclear. In this article, we report that fascin1 is highly expressed and widely distributed in mouse embryonic stem cells (mESCs), which are regulated by JAK‐STAT3 and β‐catenin. We found that the overexpression of fascin1 impairs the formation of mESC colonies via the downregulation of intercellular adhesion molecules, and that mimicking the dephosphorylated mutation of fascin1 or inhibiting phosphorylation with Gö6983 significantly enhances colony formation. Hyperphosphorylated fascin1 can promote the maintenance of pluripotency in mESCs via nuclear localization and suppressing DNA methyltransferase expression. Our findings demonstrate a novel function of fascin1, as a vital regulator, in the colony formation and pluripotency of mESCs and provide insights into the molecular mechanisms underlying embryonic stem cell self‐organization and development in vitro.

中文翻译：

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fascin1在小鼠胚胎干细胞集落形成中的作用

已知 Fascin1 通过与肌动蛋白丝结合参与癌细胞的迁移。最近的研究表明，fascin1 还调节肿瘤发生和癌症干细胞中多能性基因的维持等过程。然而，fascin1 在胚胎干细胞中的功能仍不清楚。在这篇文章中，我们报告了 fascin1 在受 JAK-STAT3 和 β-catenin 调控的小鼠胚胎干细胞 (mESCs) 中高表达并广泛分布。我们发现 fascin1 的过表达通过下调细胞间粘附分子来损害 mESC 集落的形成，并且模拟 fascin1 的去磷酸化突变或用 Gö6983 抑制磷酸化显着增强了集落形成。过度磷酸化的 fascin1 可以通过核定位和抑制 DNA 甲基转移酶表达促进 mESC 多能性的维持。我们的研究结果证明了 fascin1 作为重要调节剂在 mESC 集落形成和多能性中的新功能，并提供了对体外胚胎干细胞自组织和发育的分子机制的见解。