ArticleEnvironmental science and pollution research international2018
Transcriptome analysis to identify the Ras and Rap1 signal pathway genes involved in the response of TM3 Leydig cells exposed to zearalenone.
Article in Environmental science and pollution research international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 7 citations in OpenAlex.
- MicroRNA regulates the toxicological mechanism of four mycotoxins in vivo and in vitro.Journal of animal science and biotechnology · 2022Review
- Selenium Protects against Zearalenone-Induced Oxidative Stress and Apoptosis in the Mouse Kidney by Inhibiting Endoplasmic Reticulum Stress.Oxidative medicine and cellular longevity · 2020Article
- Analysis of the miRNA Expression Profiles in the Zearalenone-Exposed TM3 Leydig Cell Line.International journal of molecular sciences · 2019Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanism of action of zearalenone (ZEA) in inducing germ cell tumors is unclear, and little is known about the change in the transcriptome of germ cells after ZEA exposure. To explore the molecular basis of the ZEA oncogene, we examined the median lethal concentration (50 μmol/L) and pro-apoptotic effect of ZEA on TM3 Leydig cells by MTT and TUNEL assay. Subsequently, we investigated the genetic changes in the transcriptome of TM3 Leydig cells exposed to 50 μmol/L ZEA. The transcriptome sequencing results show that 772 genes are significantly down-regulated, while 204 genes are significantly up-regulated. Gene ontology (GO) enrichment analysis shows that ZEA has a major effect on the connective function, cell composition, cell cycle, and energy metabolism of the TM3 Leydig cells. Using the results of the GO and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, we select the Ras and Rap1 signaling pathways that are closely related to the occurrence of cancer. The differentially expressed genes visualized in the KEGG pathway were selected for RT-qPCR differential gene expression validation. The results show that the gene expression results are consistent with the transcriptome sequencing results. This study thus provides a theoretical molecular basis for the mechanism of ZEA carcinogenesis.
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