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Updated: Nov 19, 2025

Methods to Study Mrp4-containing Macromolecular Complexes in the Regulation of Fibroblast Migration
Published on: May 19, 2016
Atypical PKCs activate Vimentin to facilitate prostate cancer cell motility and invasion
Wishrawana S Ratnayake1, Christopher A Apostolatos1, Sloan Breedy1
1Department of Chemistry, University of South Florida , Tampa, FL, USA.
Abstract:
Atypical protein kinase C (aPKC) are involved in progression of many human cancers. Vimentin is expressed during epithelial to mesenchymal transition (EMT). Molecular dynamics of Vimentin intermediate filaments (VIFs) play a key role in metastasis. This article is an effort to provide thorough understanding of the relationship between Vimentin and aPKCs . We demonstrate that diminution of aPKCs lead to attenuate prostate cellular metastasis through the downregulation of Vimentin expression. siRNA knocked-down SNAIL1 and PRRX1 reduce aPKC activity along with Vimentin. Results suggest that aPKCs target multiple activation sites (Ser33/39/56) on Vimentin and therefore is essential for VIF dynamics regulation during the metastasis of prostate cancer cells. Understanding the aPKC related molecular mechanisms may provide a novel therapeutic path for prostate carcinoma.
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