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Protein Kinase C as a Sensor for Oxidative Stress in Tumor Promotion and Chemoprevention

  • Chapter
Oxidative Stress and Signal Transduction

Abstract

Protein kinase C (PKC) has emerged as a key enzyme that is activated by transmembrane signals such as products of phospholipid hydrolysis and Ca2+.1-5 PKC represents a family of more than 11 isoenzymes, which are divided broadly into Ca2+-dependent type (α,β,γ) and Ca2+-independent type (δ,ε,ζ, etc.).1-5 Differences in the subcellular localization as well as the expression of these isoenzymes in various cell types, enable PKC isoenzyme system to respond differentially to a wide variety of cellular stimuli.1-5 The experimental tumor promoters, phorbol esters, bind to activate PKC., which results in increased membrane association (translocation) of PKC., and ultimately leads to its down-regulation. PKC is also activated and inactivated by oxidant tumor promoters that play an important role in carcinogenesis in human settings.6-10 The unique structural aspects of PKC make it also a suitable target for the redox-sensitive cancer chemopreventive agents (antioxidants) as well as for growth-inhibiting natural products.11 This enzyme also has been shown to influence tumor cell properties such as cell motility, adhesion, invasion, and metastasis, and therefore it is involved not only in tumor promotion but also in the later events of carcinogenesis related to tumor progression.12-15 This is a crucial enzyme currently targeted for the development of cancer chemopreventive agents, antiproliferative, and antimetastatic agents.

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Authors
  1. Rayudu Gopalakrishna
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  2. Zhen-Hai Chen
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  3. Usha Gundimeda
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Editors and Affiliations

  1. University of Southern California, USA

    Henry Jay Forman  & Enrique Cadenas  & 

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Gopalakrishna, R., Chen, ZH., Gundimeda, U. (1997). Protein Kinase C as a Sensor for Oxidative Stress in Tumor Promotion and Chemoprevention. In: Forman, H.J., Cadenas, E. (eds) Oxidative Stress and Signal Transduction. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5981-8_7

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  • DOI: https://doi.org/10.1007/978-1-4615-5981-8_7

  • Publisher Name: Springer, Boston, MA

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