The Effects of Ceramides and Tram-1 Protein On Endocrine Therapy Resistant Estrogen Receptor-Positive Breast Cancer Cells
Session Number
BIO 22
Advisor(s)
Dr. Jonathan Coloff and Dr. Purab Pal,University of Illinois Chicago
Discipline
Biology
Start Date
17-4-2025 11:10 AM
End Date
17-4-2025 11:25 AM
Abstract
Endocrine therapy, the standard treatment for estrogen receptor-positive breast cancer, often fails due to drug resistance. It has been shown that this resistant phenotype is linked to lower ceramide levels and increased sensitivity to ceramide-induced cell death in the ER+ cell lines and that the protein TRAM-1 may play a crucial role in the formation of ET-resistant cells. Our research aimed to investigate the mechanisms behind ceramide sensitivity and further explore TRAM-1’s contribution to ET resistance. To do this, we conducted experiments to determine the point at which cells treated with ET drugs become ET-resistant and how the ceramide levels change during this process. We also manipulated TRAM-1 expression to see how this affected the cells' survival rates when treated with ET drugs. By clarifying the changes in ceramide levels during resistance development, and the effects of TRAM-1 on cell survival, future research may be able to use this information to create therapies that target these cells more effectively and improve the prognosis for patients with endocrine therapy resistance.
The Effects of Ceramides and Tram-1 Protein On Endocrine Therapy Resistant Estrogen Receptor-Positive Breast Cancer Cells
Endocrine therapy, the standard treatment for estrogen receptor-positive breast cancer, often fails due to drug resistance. It has been shown that this resistant phenotype is linked to lower ceramide levels and increased sensitivity to ceramide-induced cell death in the ER+ cell lines and that the protein TRAM-1 may play a crucial role in the formation of ET-resistant cells. Our research aimed to investigate the mechanisms behind ceramide sensitivity and further explore TRAM-1’s contribution to ET resistance. To do this, we conducted experiments to determine the point at which cells treated with ET drugs become ET-resistant and how the ceramide levels change during this process. We also manipulated TRAM-1 expression to see how this affected the cells' survival rates when treated with ET drugs. By clarifying the changes in ceramide levels during resistance development, and the effects of TRAM-1 on cell survival, future research may be able to use this information to create therapies that target these cells more effectively and improve the prognosis for patients with endocrine therapy resistance.