Related Experiment Video
Updated: Mar 15, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
β-arrestin1 promotes epithelial-mesenchymal transition via modulating GSK-3β/β-catenin pathway in prostate cancer
Xiaolu Duan1, Tao Zhang1, Zhenzhen Kong1
1Department of Urology, Minimally Invasive Surgery Center, The First Affiliated Hospital of Guangzhou Medical University, Guangdong Key Laboratory of Urology, Guangzhou Institute of Urology, China.
Abstract:
Recently, β-arrestin1 was indicated as a tumor promoter in prostate cancer, but its exact role in cancer metastasis still have not been well clarified. Here, our data revealed that β-arrestin1 could promote the migration and invasion of prostate cancer cells via initiating epithelial-mesenchymal transition (EMT). Mechanically, β-arrestin1 could increase the transcriptional activity and expression of β-catenin, together with Akt activity, whereas decrease the activities of GSK-3β and PP2A. In addition, β-arrestin1 could function as a scaffold protein in modulating the interactions between PP2A, Akt, GSK-3β and β-catenin. These results reveal a novel mechanism of β-arrestin1 in modulating EMT and GSK-3β/β-catenin signaling in prostate cancer, thereby suggest that assessment of β-arrestin1 may provide a potential therapeutic target for prostate cancer.
Related Concept Videos
TGF - β Signaling Pathway
PI3K/mTOR/AKT Signaling Pathway
Assembly of Signaling Complexes
Interaction domains in cell signaling
Interaction domains recognize exposed features of their binding partners containing post-translationally modified sequences,...
Amplifying Signals via Enzymatic Cascade
Intracellular Signaling Affects Focal Adhesions
Some...
The JAK-STAT Signaling Pathway

