Research Paper Volume 12, Issue 14 pp 14467—14479

The regulatory role of miR-107 in Coxsackie B3 virus replication

Figure 2. (AD) MiR-107 targeted KLF4, enhanced phosphorylation of NFκB and promoted replication of CVB3. Hela cells was infected with CVB3 after transfection with miRNA mimics or inhibitors. Cellular proteins were detected by western blot. RT-qPCR was performed to determine the mRNA level of KLF4. (E) KLF4 knockdown facilitated the phosphorylation of NFκB. Hela cells which were initially transfected with KLF4 siRNA were infected with CVB3. Protein expressions of NFκB and p-NFκB were detected by western blot analysis. (F, H) Viral titers were determined by plaque assay. (G) The overexpression of KLF4 partially suppressed the promoting effect of miR-107 on VP-1 synthesis and the phosphorylation of NFκB. Hela cells that were co-transfected with miRNA mimics and KLF4 plasmids or empty vector (Vec) were infected with CVB3 afterward. The activity of NFκB signaling was analyzed by western blot. (I) The replication level of EGFP-Iabeled CVB3 was observed in Hela cells which had been transfected with si-KLF4 or pcDNA-KLF4 (magnification, 4×).