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Protein kinase Cdelta-dependent induction of manganese superoxide dismutase gene expression by microtubule-active

K C Das1, X L Guo, C W White

  • 1Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado 80206, USA. kumunda@uthct.edu

The Journal of Biological Chemistry
|December 16, 1998
PubMed

Insights

Anticancer drugs like paclitaxel activate protein kinase C delta (PKCδ), inducing manganese superoxide dismutase (MnSOD) gene expression. This highlights PKCδ

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Bacterial lipopolysaccharide and paclitaxel (taxol) can induce manganese superoxide dismutase (MnSOD) gene expression.
  • Anticancer drugs share properties with lipopolysaccharide, suggesting a common signaling pathway.

Purpose of the Study:

  • To investigate the role of protein kinase C (PKC) in paclitaxel- and other anticancer drug-induced MnSOD gene expression.
  • To identify specific PKC isoenzymes involved in this signaling pathway.

Main Methods:

  • Treatment of human lung adenocarcinoma cells (A549) with paclitaxel, vinblastine, vincristine, and PKC activators/inhibitors.
  • Analysis of MnSOD gene expression, PKC activity, and PKC isoenzyme translocation.
  • Down-regulation of PKC using phorbol 12-myristate 13-acetate (PMA).

Main Results:

  • Paclitaxel, vinblastine, and vincristine induced MnSOD gene expression in a time- and dose-dependent manner.
  • PKC activation was crucial for drug-induced MnSOD expression, as shown by inhibition with PKC inhibitors and PKC down-regulation.
  • Anticancer drugs specifically activated PKCdelta, while other agents activated multiple PKC isoenzymes.

Conclusions:

  • Protein kinase C delta (PKCδ) plays a specific role in mediating MnSOD gene induction by anticancer drugs like paclitaxel.
  • Understanding this pathway could lead to novel therapeutic strategies targeting oxidative stress in cancer.

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