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. 2015 Jan 2;14(1):146–156. doi: 10.4161/15384101.2014.967106

Figure 2.

Figure 2.

TAZ induces the breast cancer stem cell (CSC) properties and breast tumor formation. (A) Schematic of human TAZ protein showing the TEAD-interaction domain (TEAD-B), WW domain (WW), transcription activation domain (TAD) and PDZ-binding motif. Four serine–to-alanine point mutations (S66A, S89A, S117A and S311A) are introduced into wild-type TAZ construct (TAZ-4SA); additional serine-to-alanine mutation (S51A) is introduced into TAZ-4SA construct (TAZ-4SA-S51A), which leads to the loss of interaction of TAZ with TEAD. (B) Ectopic expression of constitutively active TAZ-4SA in human non-transformed breast epithelial MCF10A cells as revealed by immunoblot. β-Actin was used as the loading control. (C) Images and quantifications of mammosphere formation of vector or TAZ-4SA transduced MCF10A cells. Bars denote standard errors (n = 6). Representative images are shown. (Scale bar, 100μm). (D) Flow cytometry analysis of CD44high/CD24low population in vector or TAZ-4SA transduced MCF10A cells. Percentage of CD44high/CD24low subpopulation is indicated. (E) Quantification of mammosphere formation in vector or TAZ-4SA transduced HMEC cells. Bars denote standard errors (n = 6). Insert: Ectopic expression of constitutively activate TAZ-4SA in human breast epithelial HMEC cells was revealed by immunoblot. β-Actin was used as the loading control. (F) TAZ-4SA-transduced MCF10A cells induce mammary tumor formation when injected into the mammary fat pad of NOD/SCID mice (n = 6). (G) Histological analysis of tumors from the TAZ-4SA injected mice. Shown are H&E and IHC staining of Ki67, pan-cytokeratin AE1/3 and human-specific vimentin.