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. 2019 Aug 19;15(10):2240–2255. doi: 10.7150/ijbs.35356

Figure 3.

Figure 3

miR-27a is responsible for the slowed migration of bystander WS1 cells. (A) The relative expression levels of miR-27a/b in WS1 cells after transfection with miR-27a/b mimics. (B) The quantification of area of the wound scratches of WS1 cells transfected with miR-27a mimics and negative control (NC), showing that transfection with miR-27a mimics significantly delayed the migration of WS1 cells. (C) The quantification of area of the wound scratches of WS1 cells transfected with miR-27b mimics and NC, showing that transfection with miR-27b mimics significantly delayed the migration of WS1 cells. (D) The alteration of miR-27a/b of bystander WS1 cells after co-culture with irradiated HaCaT cells for 12 h. (E) The relative intracellular ROS levels in WS1 cells transfected with miR-27a mimics and NC in the absence and presence of NAC, showing that NAC abolished the elevation of ROS levels in WS1 cells transfected with miR-27a mimics. (F) The quantification of area of the wound scratches of WS1 cells transfected with miR-27a mimics and NC in the presence of NAC, showing that NAC eliminated the slowed cell migration induced by miR-27a overexpression. (G) The quantification of area of the wound scratches of WS1-pCMV (left panel) and WS1-pCMV-SOD2 (right panel) cells transfected with miR-27a mimics and NC, showing that the redox status of WS1 cells affected the reduction in cell migration rate induced by miR-27a overexpression. (H) The alterations of miR-27a expression levels in irradiated HaCaT cells along with time. (I) The alterations of miR-27a expression levels in irradiated HaCaT cells pre-transfected with miR-27a inhibitors and NC, showing lack of increase in miR-27a expression in HaCaT cells transfected with miR-27a inhibitors after irradiation. (J) The intracellular ROS levels of bystander WS1 cells after co-culture with irradiated HaCaT cells pre-transfected with miR-27a inhibitors and NC, showing that down-regulation of miR-27a in irradiated HaCaT cells abolished oxidative stress in bystander WS1 cells. (K) The quantification of area of the wound scratches of bystander WS1 cells after co-culture with irradiated HaCaT cells pre-transfected with miR-27a inhibitors (right panel) and NC (left panel), showing that down-regulation of miR-27a in irradiated HaCaT cells abolished slowed migration in bystander WS1 cells. All the data represent the means ± SEM from three independent experiments (n=3). *P<0.05, **P<0.01 and ***P<0.001 compared with the relative control. NS represents "not significant".