Repression of Protein Kinase C and Stimulation of Cyclic AMP Response Elements by Fumonisin, a Fungal Encoded Toxin Which Is a Carcinogen

Chongxi Huang, Martin Dickman, Gail Henderson, Clinton Jones

Research output: Contribution to journalArticle

57 Citations (Scopus)

Abstract

Fusarium moniliforme (FM) is a major fungal pathogen of corn and is involved with stalk rot disease. FM is widely spread throughout the world, including the United States. Most strains of FM produce several mycotoxins, the most prominent of which is called fumonisin. Recent epidemiological studies indicated that ingestion of fumonisin correlates with a higher incidence of esophageal cancer in Southern and Northern Africa and China. Furthermore, fumonisin causes a neurodegenerative disease in horses, induces hepatic cancer in rats, and induces pulmonary edema in swine. Considering that high levels of fumonisin have been detected in healthy and diseased corn grown in the United States, fumonisin may pose a health threat to humans and livestock animals. Structurally, fumonisin resembles sphingolipids which are present in the membranes of animal and plant cells. At the present time, very little is known concerning the mechanism by which fumonisin elicits its carcinogenic effect Our studies indicate that fumonisin represses expression of protein kinase C and AP-1-dependent transcription. In contrast, fumonisin stimulated a simple promoter containing a single cyclic AMP response element Since fumonisin did not alter protein kinase A activity, it appears that cyclic AMP response element activation was independent of protein kinase A. It is hypothesized that the ability of fumonisin to alter signal transduction pathways plays a role in carcinogenesis.

Original languageEnglish (US)
Pages (from-to)1655-1659
Number of pages5
JournalCancer Research
Volume55
Issue number8
StatePublished - Apr 15 1995

Fingerprint

Fumonisins
Mycotoxins
Response Elements
Carcinogens
Cyclic AMP
Protein Kinase C
Fusarium
Cyclic AMP-Dependent Protein Kinases
Zea mays
Southern Africa
Northern Africa
Sphingolipids
Transcription Factor AP-1
Plant Cells
Livestock
Pulmonary Edema
Liver Neoplasms
Esophageal Neoplasms
Neurodegenerative Diseases
Horses

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Repression of Protein Kinase C and Stimulation of Cyclic AMP Response Elements by Fumonisin, a Fungal Encoded Toxin Which Is a Carcinogen. / Huang, Chongxi; Dickman, Martin; Henderson, Gail; Jones, Clinton.

In: Cancer Research, Vol. 55, No. 8, 15.04.1995, p. 1655-1659.

Research output: Contribution to journalArticle

Huang, Chongxi ; Dickman, Martin ; Henderson, Gail ; Jones, Clinton. / Repression of Protein Kinase C and Stimulation of Cyclic AMP Response Elements by Fumonisin, a Fungal Encoded Toxin Which Is a Carcinogen. In: Cancer Research. 1995 ; Vol. 55, No. 8. pp. 1655-1659.
@article{4d9f58f70c434bae91517ed9cbc2034b,
title = "Repression of Protein Kinase C and Stimulation of Cyclic AMP Response Elements by Fumonisin, a Fungal Encoded Toxin Which Is a Carcinogen",
abstract = "Fusarium moniliforme (FM) is a major fungal pathogen of corn and is involved with stalk rot disease. FM is widely spread throughout the world, including the United States. Most strains of FM produce several mycotoxins, the most prominent of which is called fumonisin. Recent epidemiological studies indicated that ingestion of fumonisin correlates with a higher incidence of esophageal cancer in Southern and Northern Africa and China. Furthermore, fumonisin causes a neurodegenerative disease in horses, induces hepatic cancer in rats, and induces pulmonary edema in swine. Considering that high levels of fumonisin have been detected in healthy and diseased corn grown in the United States, fumonisin may pose a health threat to humans and livestock animals. Structurally, fumonisin resembles sphingolipids which are present in the membranes of animal and plant cells. At the present time, very little is known concerning the mechanism by which fumonisin elicits its carcinogenic effect Our studies indicate that fumonisin represses expression of protein kinase C and AP-1-dependent transcription. In contrast, fumonisin stimulated a simple promoter containing a single cyclic AMP response element Since fumonisin did not alter protein kinase A activity, it appears that cyclic AMP response element activation was independent of protein kinase A. It is hypothesized that the ability of fumonisin to alter signal transduction pathways plays a role in carcinogenesis.",
author = "Chongxi Huang and Martin Dickman and Gail Henderson and Clinton Jones",
year = "1995",
month = "4",
day = "15",
language = "English (US)",
volume = "55",
pages = "1655--1659",
journal = "Cancer Research",
issn = "0008-5472",
publisher = "American Association for Cancer Research Inc.",
number = "8",

}

TY - JOUR

T1 - Repression of Protein Kinase C and Stimulation of Cyclic AMP Response Elements by Fumonisin, a Fungal Encoded Toxin Which Is a Carcinogen

AU - Huang, Chongxi

AU - Dickman, Martin

AU - Henderson, Gail

AU - Jones, Clinton

PY - 1995/4/15

Y1 - 1995/4/15

N2 - Fusarium moniliforme (FM) is a major fungal pathogen of corn and is involved with stalk rot disease. FM is widely spread throughout the world, including the United States. Most strains of FM produce several mycotoxins, the most prominent of which is called fumonisin. Recent epidemiological studies indicated that ingestion of fumonisin correlates with a higher incidence of esophageal cancer in Southern and Northern Africa and China. Furthermore, fumonisin causes a neurodegenerative disease in horses, induces hepatic cancer in rats, and induces pulmonary edema in swine. Considering that high levels of fumonisin have been detected in healthy and diseased corn grown in the United States, fumonisin may pose a health threat to humans and livestock animals. Structurally, fumonisin resembles sphingolipids which are present in the membranes of animal and plant cells. At the present time, very little is known concerning the mechanism by which fumonisin elicits its carcinogenic effect Our studies indicate that fumonisin represses expression of protein kinase C and AP-1-dependent transcription. In contrast, fumonisin stimulated a simple promoter containing a single cyclic AMP response element Since fumonisin did not alter protein kinase A activity, it appears that cyclic AMP response element activation was independent of protein kinase A. It is hypothesized that the ability of fumonisin to alter signal transduction pathways plays a role in carcinogenesis.

AB - Fusarium moniliforme (FM) is a major fungal pathogen of corn and is involved with stalk rot disease. FM is widely spread throughout the world, including the United States. Most strains of FM produce several mycotoxins, the most prominent of which is called fumonisin. Recent epidemiological studies indicated that ingestion of fumonisin correlates with a higher incidence of esophageal cancer in Southern and Northern Africa and China. Furthermore, fumonisin causes a neurodegenerative disease in horses, induces hepatic cancer in rats, and induces pulmonary edema in swine. Considering that high levels of fumonisin have been detected in healthy and diseased corn grown in the United States, fumonisin may pose a health threat to humans and livestock animals. Structurally, fumonisin resembles sphingolipids which are present in the membranes of animal and plant cells. At the present time, very little is known concerning the mechanism by which fumonisin elicits its carcinogenic effect Our studies indicate that fumonisin represses expression of protein kinase C and AP-1-dependent transcription. In contrast, fumonisin stimulated a simple promoter containing a single cyclic AMP response element Since fumonisin did not alter protein kinase A activity, it appears that cyclic AMP response element activation was independent of protein kinase A. It is hypothesized that the ability of fumonisin to alter signal transduction pathways plays a role in carcinogenesis.

UR - http://www.scopus.com/inward/record.url?scp=0028934299&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028934299&partnerID=8YFLogxK

M3 - Article

C2 - 7712470

AN - SCOPUS:0028934299

VL - 55

SP - 1655

EP - 1659

JO - Cancer Research

JF - Cancer Research

SN - 0008-5472

IS - 8

ER -