Treatment of MDA-MB-231 and ZR-75-30 with Vorinostat Decreases Cell Viability
Boyd,  Izzy  and Elizabeth H. Forrester.

Breast cancer is the second-leading cause of cancer death in women. HER2 is an epidermal growth factor protein that when overexpressed, can force breast cells to grow and divide unregulated, causing cancer. Histone modifications play a role in regulating gene expression by making regions of DNA active or inactive. Histone deacetylases (HDACs) play a crucial role in this process through the removal of acetyl groups on histone proteins. HDACs are often dysregulated in numerous disorders, including cancer, thereby influencing transcription of tumor suppressor genes and oncogenes. Studies have identified histone deacetylase inhibitors (HDACis) as potential therapeutic agents. However, the exact mechanism of their action is currently unknown. Because some HDAC inhibitors are FDA approved for the treatment of epilepsy and some cancers, they are of great interest as new agents are needed to improve current therapies and decrease the resistance of chemotherapy in triple-negative breast cancers. Here, we examine the effects of an HDAC pan-inhibitor, Vorinostat (SAHA ), on HER2+ and HER2- breast cancer cell lines.  Utilizing these cells lines, we analyze cell viability and expression of genes related to cell proliferation in response to treatment with various concentrations of SAHA.  In MDA-MB-231 cells, SAHA decreased viability and reduced expression of a known oncogene, BMI-1, by almost two-fold. Our results support the use of SAHA as a potential therapeutic agent for the treatment of HER2+ and HER2- breast cancer cells.

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