4.5 Article

MiR-320 and miR-494 affect cell cycles of primary murine bronchial epithelial cells exposed to benzo[a]pyrene

期刊

TOXICOLOGY IN VITRO
卷 24, 期 3, 页码 928-935

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.tiv.2009.11.013

关键词

Benzo[a]pyrene; MiR-320; MiR-494; Cell cycle; Primary murine bronchial epithelial cells

资金

  1. National Natural Science Foundation of China [30571546, 30771780]
  2. Scientific Research Foundation of the State Education Ministry [2007-24]
  3. Natural Science Foundation of Guangdong Province [07117550, 9251018201000004]
  4. Higher Education Institutions of Guangdong Province, China [06Z021]
  5. Guangzhou Bureau of Education, China [08A093]

向作者/读者索取更多资源

MicroRNAs (miRNAs) are a class of small noncoding RNA molecules with profound impact on various biological processes. Some miRNAs are involved in tumorigenesis by regulation of cell cycle progression. Here, we cultured primary murine bronchial epithelial cells and then examined the expression of miR-320 and miR-494 in cells exposed to benzo[a]pyrene (B[a]P). To better characterize roles of miR-320 and miR-494 in cell cycle progression, we used miRNA inhibitors to downregulate expression of miRNAs and determined cell cycle distribution and expression of cyclin-dependent kinases 6 (CDK6) by flow cytometric analysis. Treating cells with 1 mu M Mall) for 24 h resulted in time-dependent increases in miR-320 and miR-494 expression. Moreover, G1 arrest and downregulated expression of CDK6 were shown in the treated cells. Flow cytometric analysis indicated a relief of Cl arrest and an elevated expression of CDK6 after inhibition of the expressions of miR-320 and miR-494 in cells exposed to B[a]P. These results suggest that expression levels of miRNA-320 and miR-494, which regulate B[a]P-exposed cell cycle progression, may impact G1/S transition through CDK6, and provide further insights into functions of miRNAs in cell cycle of primary murine bronchial epithelial cells exposed to B[a]P. (C) 2009 Elsevier Ltd. All rights reserved.

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