Protein kinase C-ε protects MCF-7 cells from TNF-mediated cell death by inhibiting Bax translocation

Dongmei Lu, Usha Sivaprasad, Jie Huang, Eswar Shankar, Shavonda Morrow, Alakananda Basu

Research output: Contribution to journalArticle

28 Scopus citations

Abstract

We have previously shown that protein kinase Cε (PKCε) acts as an antiapoptotic protein and protects breast cancer MCF-7 cells from tumor necrosis factor-α (TNF)-mediated apoptosis. In the present study, we have investigated the mechanism by which PKCε inhibits TNF-induced cell death. Overexpression of wild-type PKCε (WT-PKCε) in MCF-7 cells decreased TNF-induced mitochondrial depolarization. Depletion of Bax by small interfering RNA (siRNA) attenuated TNF-induced cell death. Overexpression of PKCε in MCF-7 cells decreased dimerization of Bax and its translocation to the mitochondria. Knockdown of PKCε using siRNA induced Bax dimerization and mitochondrial translocation. PKCε was coimmunoprecipitated with Bax in MCF-7 cells. These results suggest that PKCε mediates its antiapoptotic effect partly by preventing activation and translocation of Bax to the mitochondria.

Original languageEnglish
Pages (from-to)1893-1900
Number of pages8
JournalApoptosis
Volume12
Issue number10
DOIs
StatePublished - 1 Oct 2007

Keywords

  • Apoptosis
  • Bax
  • MCF-7 cells
  • PKCε
  • TNF

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