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Fig. 3 | Cell & Bioscience

Fig. 3

From: Hsa-let-7c-5p augments enterovirus 71 replication through viral subversion of cell signaling in rhabdomyosarcoma cells

Fig. 3

EV71 replication is modulated by the hsa-let-7c-5p inhibitor. a The effect of transfection of hsa-let-7c-5pi (150 nM) into RD cells for 48 h on hsa-let-7c-5p expression was assessed by stem-loop qRT-PCR. b The virus titer is regulated by hsa-let-7c-5pi. RD cells were transfected with NCi (150 nM), hsa-let-7c-5pi (150 nM) or neither for 48 h and then infected with EV71 (MOI = 5) for 24 h. Total virus was collected from infected cells and culture supernatants and used in plaque assays. The virus titers in the cultures are expressed as PFU per milliliter. c Effects of the hsa-let-7c-5p mimic on the expression of viral RNA and (d) the viral structural protein VP1 were analyzed by qRT-PCR and Western blotting, respectively, using GAPDH as an internal control. RD cells were transfected with NCi (150 nM), hsa-let-7c-5pi (150 nM) or neither for 48 h, followed by EV71 infection (MOI = 5) for 24 h. The RD cells were subjected to mock infection, as shown in (d), to assess the specificity of the VP1 primary antibody. The lower panel in (d) shows that VP1 expression normalized to GAPDH is expressed as a fold change compared with the Mock-T group, as quantified using Image J software. e The effect of hsa-let-7c-5pi on cell viability was assessed by MTT assay. RD cells were transfected with NCi (150 nM) or hsa-let-7c-5pi (150 nM) for 48 h, followed by infection with or without EV71 (MOI = 5) for 24 h. Cell viability is expressed as percentages of the NCi-transfected and mock-infected cells, which were used as controls. *p < 0.05; **p < 0.01; ***p < 0.001; ns no significance

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