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. Author manuscript; available in PMC: 2011 Sep 15.
Published in final edited form as: Cancer Res. 2010 Aug 31;70(18):7155–7165. doi: 10.1158/0008-5472.CAN-10-0668

Figure 4. ZEB1-dependent repression of endogenous TAp73 is lost selectively in BRCA1-deficient ovarian carcinoma cells.

Figure 4

(A) Knockdown of endogenous ZEB1 (left) in wild-type (T) and BRCA1-deficient (TBR) murine ovarian carcinoma cells induces TAp73 de-repression (right) only in wild-type cells. QRT-PCR analysis 72 hours following infection with lentiviral control vector, non-specific (NS) shRNA, or ZEB1-directed shRNAs, normalized in each case to vector. Error bars show SD for two experiments in triplicate. (B) De-repression of TAp73 following endogenous ZEB1 knockdown in human BRCA1-expressing (BRCA1) but not BRCA1-deficient (Vector) ovarian carcinoma cells. Immunoblot 72 hours post lentiviral shRNA infection. (C, D) Specific binding by endogenous ZEB1 is absent in BRCA1-deficient murine (top) and human (bottom) ovarian carcinoma cells. Left, schematic diagram of the respective TAp73 genomic loci. Vertical dashes represent putative ZEB1 E-box motifs. Horizontal grey bars show fragments tested by ChIP; (*) indicates specific binding (> 100-fold over control antibody) detected by ChIP using a ZEB1-specific antibody, as shown at right. T1: wild-type BRCA1; TBR5: BRCA1-deficient murine cells. Vector: BRCA1-deficient; BRCA1: BRCA1-expresssing UWB1.289 cells. (#) Indicates no significant binding versus control antibody.

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