Atypical PKCs activate Vimentin to facilitate prostate cancer cell motility and invasion

• Main Authors: Wishrawana S. Ratnayake, Christopher A. Apostolatos, Sloan Breedy, Clare L. Dennison, Robert Hill, Mildred Acevedo-Duncan
• Format: Article
• Language: English
• Published: Taylor & Francis Group 2021-01-01
• Series: Cell Adhesion & Migration
• Subjects: pkc-ι; pkc-ζ; vimentin dynamics; phosphorylation; metastasis; prostate cancer
• Online Access: http://dx.doi.org/10.1080/19336918.2021.1882782

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.