BIM is dispensable for paclitaxel-induced apoptosis in MEFs.

<p>(A) MEFs were treated with 50 nM of paclitaxel for 48 hrs. Cell death was determined by DNA fragmentation using the Cell Death Detection ELISA^plus kit (Roche). Average values from triplicate samples are shown as representative of two independent experiments. (B) MEFs were treated with 50 nM of paclitaxel for the indicated times. Total cell extracts were subjected to Western blotting with the indicated antibodies.</p

BIM is dispensable for paclitaxel-induced apoptosis in <i>ex vivo</i> mouse mammary tumors.

<p>(A) Mouse mammary epithelial cells were treated with 1 µM of paclitaxel for 48 hrs. Cell death was determined by DNA fragmentation using the Cell Death Detection ELISA^plus kit (Roche). Average values from triplicate samples are shown as representative of two independent experiments. (B) Mouse mammary epithelial cells were treated with 1 µM of paclitaxel for the indicated time. Total cell extracts were subjected to Western blotting with the indicated antibodies.</p

Gene expression profiling analysis of salivary tumors with different p53 status.

<p>(A) Unsupervised hierarchical clustering of MMTV-<i>Hras/p53</i>^<i>+/+</i> (green), MMTV-<i>Hras/p53</i>^<i>-/-</i> (yellow), and MMTV-<i>Hras/p53</i>^{<i>R172H/R172H</i>} (red) tumors based on gene expression profiling. (B) Heatmap of the identified 188 genes through the multi-class comparison function of SAM with a low 1% False Discovery Rate (FDR) and hierarchical clustering. Red represents higher expression levels and blue represents lower levels, while white represents intermediate levels. The 6 sub-clusters identified through visual inspection are marked by color bars on the right (<i>i-vi</i>).</p

BAK plays a role in paclitaxel-induced apoptosis in human breast cancer cells.

<p>SK-BR-3 and T47D cells were infected with lentiviruses expressing shRNAs for non-targeting control or BAK. Puromycin-resistant cells were pooled after each infection. Cells were treated with 20 nM paclitaxel for SK-BR-3 or 50 nM for T47-D for the indicated times and equal amounts of total cell extracts were subjected to Western blotting with the indicated antibodies.</p

p53 protein levels in tumors of each genotype.

<p>(A) Western blot analysis of p53 using an antibody that detects both wild-type and mutant p53 (CM5). From left to right: 3 MMTV-<i>Hras/p53</i>^<i>+/+</i>, 3 MMTV-<i>Hras/p53</i>^<i>-/-</i>, and 4 MMTV-<i>Hras/p53</i>^{<i>R172H/R172H</i>} tumors. (B) Immunohistochemical staining with the CM5 anti-p53 antibody in a representative tumor of each of the three genotypes.</p

H&E staining of representative tumor of the three genotypes.

<p>Top: MMTV-<i>Hras/p53</i>^<i>+/+</i>; middle: MMTV-<i>Hras/p53</i>^<i>-/-</i>; bottom: MMTV-<i>Hras/p53</i>^{<i>R172H/R172H</i>}.</p

BAK plays a role in paclitaxel-induced apoptosis in MEFs.

<p>(A) MEFs were treated with 50 nM of paclitaxel for 48 hrs. Cell death was determined by DNA fragmentation using the Cell Death Detection ELISA^plus kit. Average values from triplicate samples are shown as representative of two independent experiments. (B) MEFs were treated with 50 nM of paclitaxel for the indicated times. Total cell extracts were subjected to Western blotting with the indicated antibodies.</p

Tumor growth responses to doxorubicin.

<p>Tumor-bearing mice were treated for nine consecutive days with doxorubicin (2 mg/kg), and tumor growth was monitored daily by caliper measurements. Tumor growth rates over time (days) measured as calculated weight (mg) for each of the three groups of tumors were plotted. Each data point represents the mean ± SEM.</p

Tumor growth rates.

<p>Tumor growth rates over time (days) measured as calculated weight (mg) for each of the three groups of tumors were plotted. Each data point represents the mean ± SEM.</p

Validation of the microarray data for sample genes by qPCR and western blotting.

<p>(A) Top: Expression levels of the <i>Cap1</i> gene in 4 salivary tumors per group measured by qPCR normalized to β-actin ± coefficient of variance (top), and by microarray analysis (bottom). (B) Protein levels of p16^Ink4a, p19^ARF, and p15^Ink4b in 5 MMTV-<i>Hras/p53</i>^<i>+/+</i> and 5 MMTV-<i>Hras/p53</i>^<i>-/-</i> tumors. β-actin was used as a loading control.</p