Belinostat Treatment of MDA-MB-231 Cells Decreases Expression of BMI-1
Hill, Lauren and Elizabeth H. Forrester

Breast cancer is now the most common type of cancer in women and is one of the leading causes of cancer-related death. New agents are needed to improve the effectiveness of current treatments and to decrease the emergence of resistance to chemotherapy drugs. Epigenetic modifications change DNA accessibility and chromatin structure, thereby controlling gene expression. Histone deacetylases (HDACs), a class of epigenetic modulators, are known to play a crucial role in cancer initiation and progression by altering the expression of genes regulating cell division. Here, we study the effects of Belinostat, an HDAC pan-inhibitor, on both HER2-positive (HER2+) and triple-negative breast cancer cell lines. The mechanism by which Belinostatdecreases cell viability is currently unknown. Utilizing ZR7530 (HER2+) and MDA-MB-231 (triple-negative) cell lines, we have performed cell viability and gene expression assays using various concentrations of Belinostat. Treatment of MDA-MB-231 with Belinostatresults in a 2-fold decrease in the expression of BMI-1, an oncogene known to be associated with advanced stages of cancer, compared to untreated cells. This data suggests that Belinostat may mediate cell proliferation via the BMI1/p16/Cyclin D1 pathway.

Click here to view poster

More Research Highlights