Professor Deng's team revealed a new mechanism of cytotoxicity of vomiting toxins

, a team of professors from South China Agricultural University and Guangdong Agricultural Bioprotein Function and Regulation Key Laboratory, revealed a new mechanism of vomiting toxin cytotoxicity. The study, published online May 7 in Biochemical Pharmacology, was selected by the international academic organization F1000Prime on July 2 as a two-star paper classified as "New Find" and rated "These data suggests that the beta-catenin is an important target for mycotoxins" (translation: results suggest that β-catenin is an important target for fungal toxins.
common, natural occurrence, difficult to control, serious threat to livestock and poultry and human health, has become a 1st world public health problem. Among them, vomiting toxin is the grain and feed detection rate and excess rate of the most serious toxin, also known as deoxychlorobacterium oleol (Deoxynivalenol, DON), belongs to the Class B single-end sporemycin family compounds, is produced by fungi such as gluten knife bacteria secondary metabolites. DON can cause serious vomiting, abdominal pain and even affect reproductive development in animals, but its molecular toxicological mechanisms and associated signaling path paths are not yet clear.
Deng Yuqun's team has long been devoted to the basic theoretical research of mycotoxin biological prevention and control, focusing on mycotoxin molecular toxicology and metabolic transformation mechanism. In view of DON's cytotoxic mechanism, the team found that the key signal transductive protein β-catenin in the classical Wnt signaling path is an important molecular target for DON to play cytotoxicity, and expounded the molecular mechanism of DON's inhibition of cell proliferation through the Wnt/β-catenin signaling path.
, below the semi-lethal dose of DON treatment cells, found a significant reduction in mRNA and protein levels of β-catenin, while proving that the reduction was not achieved through post-translation modification or nuclear transfer that affected β-catenin. THE DON β-catenin to inhibit the activity of the classic Wnt signal path on which β-catenin depends, and to lower the target genes Axin2, Cyclin D1 and c-Myc of the Wnt signal path. Where c-Myc is the regulatory factor of cell proliferation, complementing β-catenin or c-Myc protein weakens the inhibitory effect of DON on cell proliferation, indicating that β-catenin/c-Myc is the key target of DON to inhibit cell proliferation.
the classic Wnt/β-catenin signaling path path is important for the early development of embryos and the maintenance of stable state of adult tissue, and the abnormality of this path is closely related to tumors, cancer and neurodegenerative lesions. The study found that the classical Wnt signaling path is a key path in the process of DON's cytotoxicity, and β-catenin is one of the molecular targets of DON's cytotoxicity, which can help to fully reveal the molecular toxicological mechanism of DON.
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