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Fumonisin B1 induces protein kinase C translocation via direct interaction with diacylglycerol binding site

J M Yeung1, H Y Wang, D B Prelusky

  • 1Food Research Division, Food Directorate, Health Protection Branch, Health Canada, Sir Frederick Banting Research Centre, Ottawa, Ontario, Canada.

Toxicology and Applied Pharmacology
|November 1, 1996
PubMed

Insights

Fumonisin B1 (FB1) activates protein kinase C (PKC) and causes its translocation, similar to tumor promoters. This provides a mechanism for FB1

Area of Science:

  • Toxicology
  • Molecular Biology
  • Biochemistry

Background:

  • Fumonisins, particularly fumonisin B1 (FB1), are known carcinogens in rats and suspected human carcinogens.
  • The precise mechanisms underlying fumonisin-induced carcinogenesis remain poorly understood.
  • Signal transduction pathways, including protein kinase C (PKC), are implicated in carcinogenesis.

Purpose of the Study:

  • To investigate whether fumonisin B1 (FB1) affects protein kinase C (PKC) activation and translocation.
  • To elucidate the cellular mechanisms by which FB1 may contribute to carcinogenesis.

Main Methods:

  • FB1's effect on PKC activity and subcellular distribution was assessed in rat cerebrocortical slices.
  • PKC activity was measured via histone phosphorylation.
  • PKC isozyme redistribution was evaluated using immunoblotting and [3H]PDBu binding assays.

Main Results:

  • FB1 induced a concentration-dependent translocation of PKC from the cytosol to the membrane, mirroring the effect of phorbol ester (PMA).
  • FB1's action on PKC translocation was inhibited by sphingosine and 4α-phorbol 12,13-didecanoate.
  • FB1 competed with phorbol ester binding, suggesting interaction with the diacylglycerol-binding site of PKC.

Conclusions:

  • FB1 directly activates and translocates PKC, acting on the same site as phorbol esters.
  • This FB1-induced PKC activation provides a plausible cellular mechanism for its carcinogenic activity.
  • The findings highlight a critical molecular pathway involved in fumonisin toxicity and carcinogenicity.

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