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Updated: Jun 17, 2026

Inhibition of Aspergillus flavus Growth and Aflatoxin Production in Transgenic Maize Expressing the α-amylase Inhibitor from Lablab purpureus L.
Published on: February 15, 2019
Aflatoxin B1 modulates the insulin-like growth factor-2 dependent signaling axis
Tsuneyuki Ubagai1, Takane Kikuchi, Toshio Fukusato
1Department of Microbiology and Immunology, Teikyo University School of Medicine, Tokyo 173-8605, Japan.
Aflatoxin B(1) (AFB(1)) exposure can increase hepatocellular carcinoma (HCC) cell proliferation by activating the insulin-like growth factor-2 (IGF-2) signaling pathway. This study investigated AFB(1)
Area of Science:
- Hepatology
- Toxicology
- Molecular Biology
Background:
- Aflatoxin B(1) (AFB(1)) is a mycotoxin linked to hepatocellular carcinoma (HCC).
- The specific impact of AFB(1) on HCC cell behavior requires further elucidation.
- Understanding AFB(1)'s molecular mechanisms in HCC is crucial for targeted therapies.
Purpose of the Study:
- To investigate the effects of AFB(1) on gene expression in HCC cell lines.
- To determine AFB(1)'s role in regulating alpha-fetoprotein (AFP), insulin-like growth factor-2 (IGF-2), and IGF-1 receptor (IGF-1R).
- To assess AFB(1)'s influence on HCC cell proliferation via the IGF-2 signaling axis.
Main Methods:
- Culturing of four HCC cell lines (HepG2, Huh-6, Huh-7, PLC).
- Treatment with varying concentrations of AFB(1).
- Real-time PCR to quantify gene expression levels of AFP, IGF-2, and IGF-1R.
- Cell proliferation assays to measure cell number changes.
Main Results:
- AFB(1) modulated AFP expression in a cell-specific, dose-dependent manner.
- AFB(1) significantly upregulated IGF-2 and IGF-1R expression in most HCC cell lines.
- AFB(1) administration enhanced HCC cell proliferation, particularly in Huh-6 cells, correlating with IGF-2 pathway activation.
Conclusions:
- AFB(1) promotes HCC cell proliferation, likely mediated by the IGF-2 signaling pathway.
- The study highlights a potential mechanism linking AFB(1) exposure to HCC progression.
- Further research is needed to confirm the association with human hepatocarcinogenesis.
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