Fig. 4: Knockdown of MAPK1 induces apoptosis, inhibits proliferation and motility of BCa cells. | Cell Death & Disease

Fig. 4: Knockdown of MAPK1 induces apoptosis, inhibits proliferation and motility of BCa cells.

From: MiR-22 suppresses epithelial–mesenchymal transition in bladder cancer by inhibiting Snail and MAPK1/Slug/vimentin feedback loop

Fig. 4

a CCK-8 assay. BCa cells were treated with 50 nM small interfering RNA targeting human MAPK1 mRNA (named siMAPK1) or siRNA negative control (siNC) for 48 h or 72 h. The relative cell viability of the siMAPK1 treated groups was lower than that of NC treated groups (cell viability of 0 nM was regarded as 1.0), respectively. b Representative images of colony-formation assay. BCa cells were treated with 50 nM siMAPK1 or siNC for 7 days. The colony-formation rate was lower for siMAPK1 treated groups compared with siNC treated groups. c Representative images of apoptosis analysis. T24 cells were treated with 50 nM siMAPK1 or siNC for 48 h. The results showed that silencing of MAPK1 effectively induced T24 cell apoptosis. d Representative images of the 24-h transwell assay. BCa cells were pretreated with 50 nM siMAPK1 or siNC for 48 h. The results showed that knockdown of MAPK1 suppressed the migration and invasion rate of T24 and UM-UC-3 cells. e Representative images of the western blotting assay. BCa cells were treated with 50 nM siMAPK1 or siNC for 48 h. Knockdown of MAPK1 significantly regulated EMT-related proteins in BCa. f qRT-PCR analysis. UM-UC-3 cells were treated as (e). Knockdown of MAPK1 significantly regulated EMT-related mRNAs in UM-UC-3 cells. g Kaplan–Meier survival curves of BCa cohort from TCGA with different MAPK1 expression levels. Error bars represent the S.D. obtained from three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001. Scale bars = 100 μm

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