13058_2016_748_MOESM10_ESM.pdf (218.92 kB)

Additional file 10: Figure S9. of WNT4 mediates estrogen receptor signaling and endocrine resistance in invasive lobular carcinoma cell lines

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journal contribution
posted on 20.09.2016 by Matthew Sikora, Britta Jacobsen, Kevin Levine, Jian Chen, Nancy Davidson, Adrian Lee, Caroline Alexander, Steffi Oesterreich
NF-kB signaling in ILC-LTED drives WNT4-CDKN1A regulation. a Left, BCCL cells were treated with increasing concentrations of BMS-345541. Proliferation was assessed 6 days after treatment, shown as fold change vs vehicle (0.1 % dimethyl sulfoxide) control. *p < 0.0001 for parental vs LTED proliferation at 10 μM BMS (t test). Right, BCCL cells were treated with increasing concentrations of BMS. Lysates were collected 48 h posttreatment. Differential sensitivity to growth suppression at 10 μM BMS correlates with ablation of p-p65 at this concentration. b Schematic of WNT4 ERBS indicating location and sequence of predicted NF-kB/Rel binding sites. Consensus RELA (p65) and NFKB1 binding sites are shown for reference. c 134:L/E cells were reverse-transfected with 10 nM siRNA (individual constructs; numbers reference those shown in Additional file 2), and RNA was collected 60 h posttransfection. Bars represent the mean of biological triplicate ± SD. *p < 0.05 by ANOVA for expression vs siSCR (Dunnett’s multiple comparisons test). d MM134 cells were reverse-transfected with 10 nM siWNT4 or treated with 1 μM IWR or 10 μM JW for 24 h. Bars represent biological triplicate ± SD. *p < 0.05 by ANOVA (Dunnett’s multiple comparisons test) vs control. e MCF-7 and HCC1428 cells were treated and processed as described in the Fig. 5e legend. ILC and ILC-LTED data are reproduced from Fig. 5e. Data are normalized to siSCR control knockdown. (PDF 218 kb)


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