Additional file 10: Figure S9. of WNT4 mediates estrogen receptor signaling and endocrine resistance in invasive lobular carcinoma cell lines
journal contributionposted on 20.09.2016 by Matthew Sikora, Britta Jacobsen, Kevin Levine, Jian Chen, Nancy Davidson, Adrian Lee, Caroline Alexander, Steffi Oesterreich
Any type of content formally published in an academic journal, usually following a peer-review process.
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)