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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 3. A TAp73-dependent transcriptional program is required for cisplatin sensitivity in ovarian carcinoma cells and tumors.

Figure 3

(A) Ablation of TAp73 consistently induces cisplatin resistance in BRCA1-deficient but not BRCA1-reconstituted UWB1.289 cells. Lentiviral transduction expressing a control (Vec) or TAp73-directed shRNA (TAp73si) was followed by MTT assay performed at 72 hours post cisplatin. Error bars represent SD for representative experiments performed in triplicate. (B) TAp73 is important for cisplatin sensitivity in murine BRCA1-deficient (TBR) but not BRCA1 wild-type (T) carcinoma cells. Lentiviral RNAi, cisplatin treatment and MTT assay as in (A). (C) TAp73-dependent Noxa induction by cisplatin is observed selectively in BRCA1-deficient lines. Cells described in (B) were treated with cisplatin (1μM, 72 hours) followed by RNA analysis using QRT-PCR. Error bars represent SD for two experiments performed in triplicate. (D) TAp73 is highly expressed in responsive (R; > 6 months recurrence-free survival) versus unresponsive (NR) tumors. QRT-PCR analysis from unselected primary tumors, expressed as Log2 TAp73 value. Note the mean TAp73 level is 10-fold higher (23.3) in responsive cases.

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