Fig. 5: DVL2 is required for ETV4-mediated HCC metastasis and invasion. | Cell Death & Disease

Fig. 5: DVL2 is required for ETV4-mediated HCC metastasis and invasion.

From: HBx increases chromatin accessibility and ETV4 expression to regulate dishevelled-2 and promote HCC progression

Fig. 5

A In MHCC97H and HepG2.2.15 cells, ETV4 was stably knocked down, and DVL2 expression levels were detected by WB and quantitative real-time PCR (qRT–PCR) analysis. B In MHCC97H and HepG2.2.15 cells, the DVL2 expression level was detected by WB after transfection with the pcDNA3.1-ETV4 plasmid at different doses. C After the DVL2 construct was transfected into MHCC97H-LV-shETV4 and HepG2.2.15-LV-shETV4 cells, WB was performed to detect the rescue of the indicated protein expression. D WB assay showed that ETV4 regulate the protein expression levels of c-Myc and MMP7 by active β-catenin. E qPCR assays showed that ETV4 regulated c-MYC and MMP7 in transcriptional level. F In vitro, the migration and invasion capacity of MHCC97H and HepG2.2.15 cells were observed by knocking down ETV4 and then rescuing DVL2 expression. G Pearson’s correlation coefficient was conducted to evaluate the correlation between ETV4 and DVL2 mRNA level. The scatter plots showed the correlation of R = 0.4097 and P < 0.0001. H The positive relationship between the ETV4 and DVL2 expression was exhibited in 140 HBV-positive HCC patients. I The patients were divided into three groups as follows: group 1: high ETV4 + high DVL2, group 2: low ETV4 + low DVL2, and group 3: others. The combined prognosis analysis of ETV4 and DVL2 showed that group 1 had worse overall survival than the other two groups of HCC patients (P < 0.001).

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