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Toxicity study of ochratoxin A using HEK293 and HepG2 cell lines based on microRNA profiling
11 Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, China.
Abstract:
Ochratoxin A (OTA) induced DNA damage, cytotoxicity, and apoptosis in mammalian cell lines. Micro RNAs (miRNAs) are involved in physiological and developmental processes and contribute to cancer development and progression. In our study, high-throughput miRNA profiling and Kyoto Encyclopedia of Genes and Genomes analysis were applied to comparatively study the toxicity of OTA in HEK293 cells and HepG2 cells treated with 25 μM OTA for 24 h. In these two cells, the same changing miRNAs were mostly related to signal transduction pathways, whereas the different changing miRNAs were mostly related to human cancer pathways. DGCR8, Dicer1, and Drosha were significantly suppressed in HEK293 cells, indicating an impairment of miRNA biogenesis. The damage seemed more extensive in HEK293 cells. Cell models and in vivo models were also compared. Many miRNAs in vitro were markedly different from those in vivo; however, OTA toxicity was observed both in vitro and in vivo. The classification of deregulated pathways is similar. The biogenesis of miRNA was impaired in both lines. In conclusion, deregulated miRNAs in vitro are mostly related to human cancer and signal transduction pathways. The deregulated pathways in vivo are similar to those in vitro.
Insights
Ochratoxin A (OTA) causes DNA damage and apoptosis, impacting microRNA (miRNA) pathways. This study reveals OTA-induced miRNA changes linked to cancer and signal transduction, affecting miRNA biogenesis in cells and organisms.
Area of Science:
- Toxicology
- Molecular Biology
- Genomics
Background:
- Ochratoxin A (OTA) is a mycotoxin known to induce DNA damage, cytotoxicity, and apoptosis in mammalian cells.
- MicroRNAs (miRNAs) are crucial regulators of cellular processes and are implicated in cancer development and progression.
Purpose of the Study:
- To comparatively analyze the toxicity of OTA in human embryonic kidney (HEK293) and hepatocellular carcinoma (HepG2) cell lines using high-throughput miRNA profiling.
- To investigate the impact of OTA on miRNA biogenesis and identify deregulated pathways in vitro and in vivo.
Main Methods:
- High-throughput miRNA profiling was employed to analyze changes in miRNA expression in HEK293 and HepG2 cells treated with 25 μM OTA for 24 hours.
- Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis was used to identify deregulated pathways.
- Comparison between in vitro cell models and in vivo models was conducted.
Main Results:
- OTA treatment led to significant alterations in miRNA expression in both cell lines, with common changes related to signal transduction pathways and distinct changes associated with human cancer pathways.
- Suppression of DGCR8, Dicer1, and Drosha in HEK293 cells indicated impaired miRNA biogenesis, with more extensive damage observed in this cell line.
- While many miRNAs differed between in vitro and in vivo models, OTA toxicity was evident in both, and the classification of deregulated pathways showed similarities.
Conclusions:
- OTA exposure deregulates miRNAs, primarily affecting signal transduction and human cancer pathways in vitro.
- MiRNA biogenesis is impaired by OTA in both cell lines studied.
- The findings highlight OTA's toxicological impact on miRNA regulation, relevant to both cellular and organismal levels.
