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Resolution: standard / high Figure 3.
Tamoxifen promotes invasion of E-cadherin deficient MCF-7 cells. (a) MCF-7 cells were left untreated (control, 'C') or treated with transfection lipid
('L'), non-targeting (scrambled) siRNA ('NT') or E-cadherin-specific siRNA ('CDH1')
for 72 hours before assessing their invasive capacity in oestrogen-free and tamoxifen-containing
medium. siRNA-mediated suppression of E-cadherin expression alone promoted an increase
in cell invasion through Matrigel. Inclusion of tamoxifen in CDH1-treated cells resulted
in a further increase in invasive capacity. The graph is the mean of three separate
experiments. *p < 0.01 versus CDH siRNA treatment. (b) MCF-7 proliferation was determined in response to E2 ± tamoxifen and fulvestrant in
the presence and absence of E-cadherin. Data demonstrated that these cells were responsive
to both E2 and anti-oestrogens irrespective of E-cadherin presence. *p < 0.05 versus
E2 alone. (c) The growth of untreated MCF7 cells or cells treated with lipid (L), non-targeting
siRNA (NT) or CDH-1 siRNA (CDH1) over five days was determined by coulter counting.
No treatment significantly affected cellular growth over this time period. (d) MDA-MB-231 cells were treated with siRNA ± tamoxifen and changes in their invasion
determined. Tamoxifen did not have any significant effect on MDA-MB-231 cell invasion.
Borley et al. Breast Cancer Research 2008 10:R103 doi:10.1186/bcr2206 |