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. 2010 Feb 1;5(2):e8979. doi: 10.1371/journal.pone.0008979

Figure 6. CK1ε expression promotes oncogenic transformation.

Figure 6

Anchorage-independent growth of (A) human mammary epithelial or human kidney epithelial cells expressing hTERT, SV40 Early Region, and activated MEK (HMEL-MEKDD or HA1E-MEKDD) with the indicated expression constructs. Colony numbers were normalized to the control and graphs show mean ± SD of a representative experiment performed in triplicate. Immunoblotting with a CK1ε antibody to confirm expression is shown in middle panel. Lower panel shows tumor formation of HA1E-MEKDD cells expressing myristoylated CK1ε. (B) β-catenin is required for anchorage-independent growth of HA1E-MEKDD cells expressing myristoylated CK1ε. Colony numbers were normalized to the GFP control and graph shows mean ± SD of a representative experiment performed in triplicate. Representative images from each condition are shown in lower panel. (C) Differential effect of CTNNB1 suppression on the proliferation of HA1E-MEKDD cells expressing CK1ε versus GFP control. P values calculated for shBCAT A and shBCAT B for MF-CK1e-expressing cells are 0.034 and 0.038 respectively. P values for shBCAT A and shBCAT B for MF-GFP-expressing cells are 0.33 and 0.10 respectively. (D) Expression of constitutive active S33Y β-catenin mutant can substitute for myristyolated-CK1ε in promoting anchorage-independent growth in human mammary epithelial cells expressing hTERT, SV40 Early Region and activated MEK.