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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: CXCL12/CXCR4 promotes inflammation-driven colorectal cancer progression through activation of RhoA signaling by sponging miR-133a-3p

Fig. 5

The downregulation of miR-133a-3p by activation of CXCL12/CXCR4 plays a crucial role in the regulation of target gene RhoA. a Heatmaps of differentially expressed miRNAs in HCT116 cells overexpressing CXCR4 or induced by 50 ng/μl CXCL12 for 12 h by miRNA-sequencing. GO analysis of the functions of target genes of differentially expressed miRNAs. b, c HCT116 and SW620 cells infected with lentivirus-CXCR4 were treated with or without 50 ng/μl CXCL12 for 24 h. These cells were also transfected with 200 nM siRNA of CXCR4 for 48 h. Western blot was performed to detect the expression of CXCR4. RT-qPCR was performed to determine the expression of miR-133a-3p. *P < 0.05 vs. control. d-f HCT116 and SW620 cells were transfected with 100 nM miR-133a-3p mimics (133 m) or inhibitors (133i) for 48 h. The levels of miR-133a-3p and RhoA were determined by RT-qPCR assay and Western blot. g HCT116 cells were transfected with luciferase constructs and miR-133a-3p mimics. The comparison of luciferase activity of wild-type (WT) and mutant (MUT) RhoA-3’UTR constructs was performed 36 h after transfection. Data was normalized to renilla activity. *P < 0.05 vs. negative control (NC)

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