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. 2015 Mar 23;17(3):317–328. doi: 10.1016/j.neo.2015.02.003

Figure 7.

Figure 7

Deptor promotes breast cancer survival through coupling to survivin expression. (A) Caspase-Glo 3/7 analyses were performed to monitor the extent of anoikis and caspase-3/7 activation in control (MT) and Deptor-expressing MDA-MB-231 cells. Data are the mean (± SE; n = 3; *P < .02). (B) Deptor expression induces that of survivin in MDA-MB-231 cells cultured over poly-HEMA–coated plates. Immunoblots are representative of three independent experiments. (C) Immunohistochemical staining of survivin in pulmonary lesions produced by parental (MT) and Deptor-expressing MDA-MD-231 cells inoculated into mice used in Figure 6. (D) Deptor expression induces that of survivin in 4T07 cells cultured over poly-HEMA–coated plates. Immunoblots are representative of two independent experiments. (E) Oncomine data correlating Deptor expression to paclitaxel responsiveness using Barretina Breast Cancer Cell Line. (F) Caspase-Glo 3/7 analyses of paclitaxel-treated (50 nM) control (MT) and Deptor-expressing MDA-MB-231 cells. Data are the mean (± SEM; n = 2; *P < .002). (G) Paclitaxel treatment significantly induces survivin mRNA expression in Deptor-expressing MDA-MB-231 cells as compared to their parental counterparts. Data are the mean (± SEM; n = 4; *P < .04). (H) MDA-MB-231 cells were depleted of survivin expression using two independent lentiviral shRNAs against survivin (shSv1 and shSv2). (I) Annexin V–fluorescein isothiocyanate staining of parental (MT), Deptor-expressing (Deptor), or Deptor-expressing/survivin-deficient (Deptor shSv1/2) MDA-MB-231 cells treated with either paclitaxel (50 nM) or doxorubicin (50 nM) as indicated. The top panels show representative histograms obtained in two independent experiments, while the bottom panel shows the mean (± SEM; n = 2; *P < .05).