The Scribble-Rac1 signaling axis drives epithelial cell motility and contributes to diffuse adenomyosis pathogenesis

IF 3.5 3区生物学 Q3 CELL BIOLOGY

Experimental cell research Pub Date : 2025-06-15 DOI:10.1016/j.yexcr.2025.114654

Xiaoping He , Yaoming Peng , Haiou Liu , Congjian Xu

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引用次数: 0

Abstract

Purpose

The study was designed to investigate whether estrogen regulates cell migration through cell polarity signaling and contributes to adenomyosis development.

Methods

In vitro study, Ishikawa cells received different treatments, Western Blot was used to detect the expression of adhesion factors and cytoskeletal proteins. Pseudopodia formation was assessed by cell immunofluorescence staining. Scratch test and transwell invasion test were used to detect the changes in Ishikawa cell migration and invasion.

Results

Scribble expression in Ishikawa cells is down-regulated by estrogen, leading to reduced expression of adhesion factors, increased expression of cytoskeletal proteins, enhanced pseudopodia formation, and elevated cell motility and invasion. Molecular mechanism research suggests that reduced Scribble expression may promote cell motility and invasion through activation of the Rac1-IRSp53-WAVE2 signaling pathway.

Conclusions

Scribble downregulation may serve as an indicator of adenomyosis severity. Its reduction alters cytoskeletal protein expression, enhancing cell motility. Mechanistically, Scribble downregulation likely activates Rac1, triggering the Rac1/IRSp53/WAVE2 pathway, which promotes pseudopodia formation and increases cell migration. These insights provide a theoretical basis for understanding the pathogenesis of adenomyosis.

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Scribble-Rac1信号轴驱动上皮细胞运动并参与弥漫性子宫腺肌症发病机制

目的探讨雌激素是否通过细胞极性信号传导调节细胞迁移并促进子宫腺肌症发育。方法在体外研究中，石川细胞经不同处理后，采用Western Blot检测黏附因子和细胞骨架蛋白的表达。细胞免疫荧光染色观察假足形成情况。采用划痕试验和transwell侵袭试验检测石川细胞迁移和侵袭的变化。结果雌激素可下调石川细胞scribble表达，导致黏附因子表达减少，细胞骨架蛋白表达增加，假足形成增强，细胞运动和侵袭能力增强。分子机制研究表明Scribble表达减少可能通过激活Rac1-IRSp53-WAVE2信号通路促进细胞运动和侵袭。结论scribble下调可作为子宫腺肌症严重程度的指标。它的减少改变了细胞骨架蛋白的表达，增强了细胞的运动性。机制上，Scribble下调可能激活了Rac1，触发了Rac1/IRSp53/WAVE2通路，从而促进假足形成并增加细胞迁移。这些发现为了解子宫腺肌症的发病机制提供了理论基础。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Experimental cell research 医学-细胞生物学

CiteScore

7.20

自引率

0.00%

发文量

295

审稿时长

30 days

期刊介绍： Our scope includes but is not limited to areas such as: Chromosome biology; Chromatin and epigenetics; DNA repair; Gene regulation; Nuclear import-export; RNA processing; Non-coding RNAs; Organelle biology; The cytoskeleton; Intracellular trafficking; Cell-cell and cell-matrix interactions; Cell motility and migration; Cell proliferation; Cellular differentiation; Signal transduction; Programmed cell death.