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. 2017 Nov 21;7:15929. doi: 10.1038/s41598-017-16175-x

Figure 4.

Figure 4

MiR-30e regulates cell proliferation, migration, invasion and increases chemosensitivity of MDA-MB-231 cells to paclitaxel by inhibiting its target IRS1. (a) Overexpression of miR-30e arrested cell proliferation, but this was rescued upon coexpression of exogenous IRS1 in MDA-MB-231 cells. (b) Cells were treated as above. A sterile 200 μl pipette tip was used to scratch the cells to form a wound. The wound gaps were photographed (top) and measured (bottom). Forced expression of miR-30e also markedly reduced the wound-healing rate, and overexpression of IRS1 reverses the inhibitory effects of miR-30e. (c) MiR-30e overexpression decreased cell invasion in MDA-MB-231 cells. Cells were transfected with miR-30e followed by IRS1 transfection. All cells were subjected to a Matrigel invasion assay. (d) MDA-MB-231 cells stably expressing miR-NC or miR-30e were pretreated with various concentration of paclitaxel for 48 h, and subjected to CCK8 Assay. (e,f) MDA-MB-231 cells stably expressing miR-NC, miR-30e or miR-30e forced expression of IRS1 were pretreated with 4 nM of paclitaxel for definite time points, and subjected to CCK8 Assay, apoptosis analysis by flow cytometry. (g) MDA-MB-231cells stably expressing miR-NC or miR-30e were transfected with 2 μg pCMV6 vector or pCMV6–IRS1 plasmid and cultured with or without paclitaxel. After 72 h, the relative caspase-3 activities were determined. Data represent mean ± SD. of 3 replicates. * or # indicated significant difference at P < 0.05. **Indicated significant difference at P < 0.01. *Indicates significant difference compared to control; #indicates significant difference compared to miR-30e plus IRS1 treatment.