Dicer knockdown induces fibronectin-1 expression in HEK293T cells via induction of Egr1 |
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| Authors: | Kai-Fu Tang Guan-Bin Song Yi-Song Shi Lin Yuan Yong-Hua Li |
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| Affiliation: | 1. Key Laboratory of Biorheological Science and Technology (Chongqing University), Ministry of Education, College of Bioengineering, Chongqing University, Chongqing 400044, PR China;2. Department of cardiology, Southwest Hospital, Third Military Medical University, Chongqing 400038, PR China |
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| Abstract: | BackgroundDicer is a multidomain ribonuclease III enzyme involved in the biogenesis of microRNAs (miRNAs) and small interfering RNAs (siRNAs); depletion of Dicer was found to impair the migration of endothelial cells.MethodssiRNA transfection, cell migration assay, real-time RT–PCR, chromatin immunoprecipitation, Western blotting, ELISA, caspase-3 activity assay, and annexin-V–FITC assay were utilized.ResultsKnockdown of Dicer impairs the migratory capacity of HEK293T cells and induces fibronectin-1. The upregulation of fibronectin-1 is dependent on Egr1. Fibronectin-1/Dicer double-knockdown cells showed a marked increase in apoptosis compared with fibronectin-1 single knockdown cells.ConclusionsDecreased Dicer expression induces fibronectin-1 expression via an Egr1-dependent manner.General significanceOur data suggest that upregulation of fibronectin-1 protects Dicer knockdown HEK293T cells against apoptosis. |
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| Keywords: | Fibronectin-1 Dicer Egr1 Cell migration |
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