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We have previously shown that PTHrP(38–94) amide restrains growth and invasion  in vitro , causes striking toxicity and accelerates death of some breast cancer cell lines, the most responsive being MDA-MB231, for which tumorigenesis was also attenuated  in vivo . We have also demonstrated that mid-region PTHrP gains access to the nuclear compartment of these cells and displays DNA-binding properties  in vitro  by recognizing targets in both cellular chromatin and isolated oligonucleotides. Here, we examined whether PTHrP(38–94) amide was able to modulate gene expression of MDA-MB231 cells, employing a combination of conventional, differential display and semi-quantitative multiplex PCR techniques. The results obtained provide first evidence that PTHrP(38–94) amide can affect gene expression in tumor cells, identifying  A4-differentiation protein/PLP2  as up-regulated, and  HOX7/MSX1 ,  COX6C ,  FZD6 ,  OXR1  and  TMCO4  as down-regulated genes in treated cells, and suggest that the cytotoxic activity of the peptide can be ascribed, at least in part, to such transcriptional reprogramming.

Mid-region parathyroid hormone-related protein (PTHrP) and gene expression of MDA-MB231 breast cancer cells