Genome-wide miRNA-profiling of aflatoxin B1-induced hepatic injury using deep sequencing

Toxicol Lett. 2014 Apr 21;226(2):140-9. doi: 10.1016/j.toxlet.2014.01.021. Epub 2014 Jan 26.

Abstract

Aflatoxin B1 is a potent carcinogen which can induce** hepatocellular carcinoma (HCC) in mammals. Though microRNAs are known to play important roles in tumorigenesis, the functional complexity of microRNAs in AFB1-induced hepatocellular tumorigenesis has not yet been elucidated. Here, we applied Illumina deep sequencing technology for high-throughput profiling of microRNA in rat liver tissue before and after treatment with aflatoxin B1. Analysis of mature miRNAs from different arms of pre-miRNAs allowed us to identify the predominant form of miRNA. We studied the differential expression profile of miRNAs in two libraries, identifying several cancer-related microRNAs which exhibit abnormal expression. KEGG analysis indicated that predicted target genes of differentially expressed miRNAs are involved in cancer-related pathways. Bioinformatic analysis predicted 16 potential novel miRNAs. Our work provides new insights at the miRNA level into AFB1-induced hepatic injury which may lead to HCC.

Keywords: Aflatoxin B1; Hepatocellular carcinoma; High-throughput sequencing; MicroRNA.

MeSH terms

  • Aflatoxin B1 / toxicity*
  • Animals
  • Base Sequence
  • Carcinoma, Hepatocellular / chemistry
  • Carcinoma, Hepatocellular / genetics
  • Cell Transformation, Neoplastic / genetics
  • Chemical and Drug Induced Liver Injury / etiology
  • Chemical and Drug Induced Liver Injury / genetics*
  • Chemical and Drug Induced Liver Injury / pathology
  • Computational Biology
  • Databases, Genetic
  • Gene Expression Profiling / methods*
  • Gene Expression Regulation, Neoplastic
  • Genetic Markers
  • High-Throughput Nucleotide Sequencing*
  • Liver / metabolism*
  • Liver / pathology
  • Liver Neoplasms / chemically induced
  • Liver Neoplasms / genetics
  • Male
  • MicroRNAs / metabolism*
  • Molecular Sequence Data
  • RNA Precursors / metabolism*
  • Rats
  • Rats, Inbred F344
  • Reproducibility of Results

Substances

  • Genetic Markers
  • MicroRNAs
  • RNA Precursors
  • Aflatoxin B1