Androgens repress Bcl-2 expression via activation of the retinoblastoma (RB) protein in prostate cancer cells.

The oncogene Bcl-2 is upregulated frequently in prostate tumors following androgen ablation therapy, and Bcl-2 overexpression may contribute to the androgen-refractory relapse of the disease. However, the molecular mechanism underlying androgenic regulation of Bcl-2 in prostate cancer cells is understood poorly. In this study, we demonstrated that no androgen response element (ARE) was identified in the androgen-regulated region of the P1 promoter of Bcl-2 gene, whereas, we provided evidence that the androgenic effect is mediated by E2F1 protein through a putative E2F-binding site in the promoter.

Increased arthritis severity in mice coinfected with Borrelia burgdorferi and Babesia microti.

Increased severity of disease and persistence of symptoms have been recently reported in some patients with simultaneous infection of Borrelia burgdorferi and Babesia microti in the northeastern and northern midwest United States. This study used a murine model to examine whether defined disease conditions such as arthritis and carditis differed in severity in mice infected solely with B. burgdorferi and in mice coinfected with B.

Disruption of androgen receptor function inhibits proliferation of androgen-refractory prostate cancer cells.

Prostate cancer cells depend on androgens and the androgen receptor (AR) for survival. However, after androgen ablation therapy, tumors relapse to an androgen-refractory state. To determine whether the androgen receptor is critical for proliferation of androgen-refractory prostate cancer cells, we disrupted the activity of the androgen receptor with an antibody and an AR mRNA hammerhead ribozyme in the following cell lines: LNCaP (androgen-sensitive), LNCaP-Rf and LNCaP-C4 (androgen-refractory), and DU-145 (androgen-insensitive).