Protein Kinase C-ε Promotes EMT in Breast Cancer

Breast Cancer: Basic and Clinical Research

Original Research

Kirti Jain¹  Alakananda Basu¹ 

[1] Department of Molecular and Medical Genetics, University of North Texas Health Science Center, Institute for Cancer Research, Fort Worth, TX, USA.;Focused on Resources for her Health Education and Research, Fort Worth, TX, USA.;

关键词: PKCε;    EMT;    breast cancer;   

DOI  :  10.4137/BCBCR.S13640

 received in 2013-11-13, accepted in 2013-12-16,  发布年份 2014

来源: Sage Journals

【 摘 要 】

Protein kinase C (PKC), a family of serine/threonine kinases, plays critical roles in signal transduction and cell regulation. PKCε, a member of the novel PKC family, is known to be a transforming oncogene and a tumor biomarker for aggressive breast cancers. In this study, we examined the involvement of PKCε in epithelial to mesenchymal transition (EMT), the process that leads the way to metastasis. Overexpression of PKCε was sufficient to induce a mesenchymal phenotype in non-tumorigenic mammary epithelial MCF-10 A cells. This was accompanied by a decrease in the epithelial markers, such as E-cadherin, zonula occludens (ZO)-1, and claudin-1, and an increase in mesenchymal marker vimentin. Transforming growth factor β (TGFβ) induced Snail expression and mesenchymal morphology in MCF-10 A cells, and these effects were partially reversed by the PKCε knockdown. PKCε also mediated cell migration and anoikis resistance, which are hallmarks of EMT. Thus, our study demonstrates that PKCε is an important mediator of EMT in breast cancer.

【 授权许可】

CC BY-NC   
© 2014 SAGE Publications.

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