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

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.

• Authors: Wishrawana S Ratnayake, Christopher A Apostolatos, Sloan Breedy, Clare L Dennison, Robert Hill, Mildred Acevedo-Duncan
• Journal: Cell adhesion & migration (Cell Adh Migr) Vol. 15 Issue 1 Pg. 37-57 (12 2021) ISSN: 1933-6926 [Electronic] United States
• PMID: 33525953 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Homeodomain Proteins
• PRRX1 protein, human
• Vimentin

Topics

• Cell Line, Tumor
• Cell Movement
• Epithelial-Mesenchymal Transition (genetics)
• Homeodomain Proteins
• Humans
• Intermediate Filaments
• Male
• Prostatic Neoplasms (genetics)
• Vimentin (genetics)