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Downregulation of CCND1 and CDK6 by miR‐34a induces cell cycle arrest
Author(s) -
Sun Fang,
Fu Hanjiang,
Liu Qin,
Tie Yi,
Zhu Jie,
Xing Ruiyun,
Sun Zhixian,
Zheng Xiaofei
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.03.057
Subject(s) - cyclin dependent kinase 6 , cyclin d1 , cell cycle , microrna , downregulation and upregulation , messenger rna , cell cycle checkpoint , microbiology and biotechnology , retinoblastoma protein , translation (biology) , ectopic expression , cyclin dependent kinase , chemistry , biology , cancer research , apoptosis , gene , biochemistry
miRNAs regulate gene expression by inhibiting translation or by targeting messenger RNA (mRNA) for degradation in a post‐transcriptional fashion. In the present study, we show that ectopic expression of miR‐34a reduces both mRNA and protein levels of cyclin D1 (CCND1) and cyclin‐dependent kinase 6 (CDK6). We also demonstrate that miR‐34a targets the 3′‐untranslated mRNA region of CCND1 as well as CDK6, which in turn interferes with phosphorylation of retinoblastoma. In addition, we show that overexpression of miR‐34a induces a significant G1 cell‐cycle arrest in the A549 cell line. Taken together, our data suggest that the effects of miR‐34a on G1 cell cycle arrest are through the down‐regulation of CCND1 and CDK6, which is associated with other targets of miR‐34a either additively or synergistically.