Submission Date

7-23-2025

Document Type

Paper

Department

Biology

Faculty Mentor

Ramesh Dasari

Comments

Presented during the 27th Annual Summer Fellows Symposium, July 18, 2025 at Ursinus College.

Project Description

Breast cancer is the leading cause of cancer-related deaths among women worldwide and the second most common cause of cancer deaths in women in the United States. Genetic variants that increase the risk of breast cancer include mutations in the breast cancer susceptibility genes 1 and 2 (BRCA1 and BRCA2). Apoptosis, or programmed cell death, is a natural process that helps the body remove aged cells. However, in cancer, deregulated apoptotic signaling—especially the activation of anti-apoptotic mechanisms—enables cancer cells to evade this process, leading to uncontrolled proliferation, tumor survival, therapeutic resistance, and cancer recurrence. Most anti-cancer drugs function as chemotherapeutic agents by inhibiting the proliferation of cancer cells and inducing apoptosis. This study investigates the apoptotic induction activity of carboplatin, a cytotoxic agent, and tucidinostat (chidamide), an HDAC-inhibiting chemotherapy drug, in breast cancer cells (BT-549). We determined the IC50 values for both compounds were evaluated, and their synergistic and antagonistic effects on BT-549 cells were assessed. The cytotoxic effects of these compounds, both individually and in combination, were assessed using the MTT assay. The impact of these drugs on metabolic functions was analyzed using the clonogenic assay and cell death assays.

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