Protein kinase C-ε promotes EMT in breast cancer

Kirti Jain, Alakananda Basu

Research output: Contribution to journalArticleResearchpeer-review

15 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)61-67
Number of pages7
JournalBreast Cancer: Basic and Clinical Research
Volume8
Issue number1
DOIs
StatePublished - 26 Mar 2014

Fingerprint

Epithelial-Mesenchymal Transition
Protein Kinase C
Breast Neoplasms
Claudin-1
Anoikis
Tight Junctions
Protein-Serine-Threonine Kinases
Snails
Transforming Growth Factors
Vimentin
Cadherins
Tumor Biomarkers
Oncogenes
Cell Movement
Signal Transduction
Breast
Neoplasm Metastasis
Phenotype

Keywords

  • Breast cancer
  • EMT
  • PKCε

Cite this

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abstract = "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.",
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Protein kinase C-ε promotes EMT in breast cancer. / Jain, Kirti; Basu, Alakananda.

In: Breast Cancer: Basic and Clinical Research, Vol. 8, No. 1, 26.03.2014, p. 61-67.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

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AU - Basu, Alakananda

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AB - 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.

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