PRIMA-1MET Does Not Restore Vitamin D Sensitivity to MDA-MB-231 and MDA-MB-468 Triple-Negative Breast Cancer Cells

Vitamin D is a steroidhormone that causes growth suppression incultured cells. We had previously discovered that the triple-negativebreast cancer cell lines MDA-MB-231 and MDA-MB-468 did not have growthsuppression with vitamin D, while MCF-7 did. MCF-7 cells are not triple-negativeand have wild-type p53. Both MDA-MB-231 and MDA-MB-468 have mutationsin p53 and these mutations were a possible explanation for the lackof growth suppression with vitamin D. Our hypothesis was that reactivationof p53 in the triple-negative cell lines would cause them to becomesensitive to vitamin D. We chose to use the small molecule PRIMA-1(MET) to reactivate p53 as it has been previously shown to restorefunction to the p53 mutants present in MB-231 and MB-468. We thenmeasured the ability of vitamin D and its analogues calcipotriol andEB1089 to suppress growth in the presence of PRIMA-1(MET). Here, we show that while PRIMA-1(MET) can kill the breastcancer cells investigated in this study, it does not restore theirsensitivity to vitamin D or its analogues.