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. 2008 Apr;172(4):893–904. doi: 10.2353/ajpath.2008.070899

Figure 2.

Figure 2

siRNA- and shRNA-mediated disruption of CCN6 down-regulates E-cadherin in benign breast and nonbreast epithelial cells. A: CCN6 protein levels of HME cells, MCF10A benign breast cells, and a panel of breast cancer cell lines. B: Stable down-regulation of CCN6 in HME cells by siRNA and shRNA. Using these two strategies, CCN6 protein levels were reduced in HME cells. C: CCN6 inhibition induces EMT of HME cells. Phase contrast microscopy showing that whereas HME controls are oval, CCN6-deficient HME cells (either by si- or shRNA) have cytoplasmic extensions and mesenchymal cell shape. D: CCN6-deficient clones have significantly reduced levels of E-cadherin protein (top) and E-cadherin mRNA (bottom) when compared with the empty vector-transfected HME cells. E: Inhibition of CCN6 markedly reduces the activity of the E-cadherin gene promoter. The effect of CCN6 inhibition on the activity of the E-cadherin promoter was assessed on HME, MCF10A, and HEK293 cells with the reporter construct, Ecad(−108)-Luc, which contains the wild-type promoter sequence from nucleotides −108 to +125 of the endogenous E-cadherin promoter.