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MiR-3940-5p enhances homologous recombination after DSB in Cr(VI) exposed 16HBE cell

  • Yang Li
  • , Guiping Hu
  • , Ping Li
  • , Shichuan Tang
  • , Ji Zhang
  • , Guang Jia*
  • *此作品的通讯作者
  • Peking University
  • Beijing Academy of Science and Technology
  • Shenzhen Center for Disease Control and Prevention

科研成果: 期刊稿件文章同行评审

摘要

Hexavalent chromium (Cr(VI)) is a well-recognized human carcinogen, yet the molecular mechanisms by which cause human cancer are still not well understood. MicroRNAs (miRNAs), which are small non-coding RNAs, are involved in carcinogenesis and DNA damage repair. Previous occupational population study showed that hexavalent chromium (Cr(VI)) downregulated plasma miR-3940-5p level, and a low miR-3940-5p level was associated with high XRCC2 expression in lymphocytes, indicating that miR-3940-5p maybe play a protective effect in Cr(VI) induced DNA damage. Here we investigated miR-3940-5p expression and its roles in DNA repair in Cr(VI)-treated 16HBE cells. miR-3940-5p change was detected by qRT-PCR. Rad51 foci formation and double strand break (DSB) were investigated to assess homologous recombination repair (HR) capacity by Immunofluorescent assay and Neutral Comet assay. XRCC2 expression was also evaluated after miRNA oligonucleotides transfection using Western blot. Cr(VI) treatment suppressed miR-3940-5p level in 16HBE cells. miR-3904-5p mimic downregulated XRCC2 expression. As a result, the formation of Rad51-foci was inhibited and DSB repair was prolonged. The results indicate that miR-3940-5p plays a protective effect in Cr(VI) induced DNA damage.

源语言英语
页(从-至)1-6
页数6
期刊Toxicology
344-346
DOI
出版状态已出版 - 17 2月 2016
已对外发布

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    可持续发展目标 3 良好健康与福祉

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