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

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.

Automated summary

The study reveals that aPKC regulates the metastasis of prostate cancer cells by controlling Vimentin expression. Knocking down SNAIL1 and PRRX1 also reduces aPKC activity and Vimentin levels, suggesting the critical role of aPKC in VIF dynamics regulation during prostate cancer cell metastasis.