17α-Ethynyl-5α-androstane-3α, 17β-diol Treatment of MNU-Induced Mammary Cancer in Rats
Figure 5
Expression of proapoptosis and differentiation genes in tumors. Seven-week-old female Lewis rats were treated with a single IP injection of 50 mg/kg MNU. Tumors developed for 90 days, prior to treatment () for 14 days with cyclodextrin vehicle daily, or 6.6 mg HE3235 daily. Gene expression was measured by RT-PCR. The graphs show ratios of gene expression in HE3235 (6.6 mg) treated tumor samples relative to vehicle treated, normalized to β-actin. Amphiregulin (Areg), androgen receptor (AR), tumor protein 53 (p53), Bcl2 antagonist of cell death (Bad), apoptosis regulator BAX (bax), B-cell CLL/lymphoma 2 (Bcl-2), caspase 3 (Casp3), caspase 8 (Casp8), caspase 9 (Casp9), Cyclin D1 (Ccnd1), estrogen receptor alpha (ERα), estrogen receptor beta (ERβ), progesterone receptor isoform A (PR-A), and vascular endothelial growth factor (VEGF). HE3235 treatment upregulates proapoptotic genes in tumors and downregulates tumor proliferation and malignancy genes.
