Cover caption

Abstract

The emergence of cells resistant to therapy is a problem shared by microbiologists, virologists and oncologists. In cancer cells, the upregulation of genes such as MDR, which encodes the multi-drug resistant transporter, results in chemotherapeutic agents being shuttled out of the cells before the agent is able to accomplish its task. An interesting approach to overcoming this resistance is to inhibit such a gene.  One purported sensor of toxins, both xenobiotic and endobiotic, is hPXT. In the current issue of Cancer Biology & Therapy, Chen and colleagues examine the role of hPXR in the response of breast cancer cells to chemotherapy when hPXR is activated or inhibited. Because hPXR is an orphan receptor able to transactivate drug-metabolizing enzymes as well as MDR, the authors look at the localization of hPXR in MDA-MB-231 breast cancer cells treated with the hPXR agonist, SR12813. The cover shows that in these SR12813 treated cells, hPXR moves from the cytoplasm (where it is seen in mock treated cells, see Figure 2bii), to the nucleus (green). Cells are counterstained (red) with phalloidin to stain actin filaments. To learn more about the effects of hPXR on the response of breast cancer cells treated with chemotherapeutic agents, see the manuscript by Chen and colleagues.