Endotoxin Triggers Tumor Initiation Events in Nontumorigenic Breast Epithelial Cells and Enhances Invasion-Related Phenotype in Pretumorigenic and Tumorigenic Breast Epithelial Cells

Figure 3

Long-term endotoxin treatment enhances migration of normal mouse mammary epithelial cells (SCp2) and human breast cancer cells (MCF-7 and MDA-MB-231). (a) Wound healing assay showed enhanced replenishment of wound area with migrating SCp2 cells upon long-term exposure (for one month) to 0.1 µg/ml ET, as opposed to short-term exposure (for 48 hours after wounding) or untreated controls (0 µg/ml). (b) Bar graph shows the percentage of the replenished wound area with migrating SCp2 cells upon short-term and long-term exposure to 0.1 µg/ml ET relative to untreated controls, for 48 hours after wounding. (c) Long-term exposure to 1 µg/ml ET increased the proliferation rate of MCF-7 and (d) MDA-MB-231 cells, as opposed to short-term exposure, where the increase in cell count was not significant when compared to untreated controls (0 µg/ml). Wound healing assay showed enhanced migration of (e, f) MCF-7 upon short (albeit marginal) and long-term exposures and (g, h) MDA-MB-231 upon long-term exposure to 1 µg/ml ET, when compared to untreated controls (0 µg/ml). Scale bar = 100 µm. Each bar represents triplicate analyses of mean ± SD. ; ; compared to the untreated control.

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