A Novel Treatment for Triple-negative Breast Cancer: NS1643
Session Number
Project ID: MEDH 34
Advisor(s)
Richard D. Minshall, Samuel Man Lee, University of Illinois at Chicago
Discipline
Medical and Health Sciences
Start Date
17-4-2024 10:00 AM
End Date
17-4-2024 10:15 AM
Abstract
Triple Negative Breast Cancer (TNBC) remains a significant cause of mortality, with 150,000 deaths annually worldwide. To address this staggering statistic, a comprehensive literature review was undertaken to explore TNBC treatments, revealing phosphorylated caveolin-1 (Cav-1) expression as pivotal in breast cancer metastasis. Interestingly, human triple-negative breast cancer cells (MDA- 231) uniquely overexpress the K+ channel Kv11.1, providing a potential drug target not present in normal breast epithelia. Treatment of MDA-231 cells with Kv11.1 activator NS1643 induced the dephosphorylation of Cav-1 and its resultant dissociation of β-catenin, a crucial regulatory protein for assembly of cell-cell adhesion complexes, towards desmosomal proteins. This experiment aimed to test if MDA-231 cells treated with NS1643 will reduce tumor cell migration and promote contact inhibition via liberation of β- catenin and its resultant interactions with desmosomal proteins. The procedure involved treating MDA-231 cells with NS1643, conducting Western blot analysis of desmosomal proteins, and measuring electrical resistance of cell monolayers grown on gold-plated microelectrodes with an epithelial cell impedance system. Results thus far indicate NS1643 rapidly increases the expression of desmosomal proteins and monolayer resistance within 24 hrs. By uncovering a novel pharmacological approach to inhibit TNBC metastasis, this study aims to not only extend patients' lives but also enhance their overall quality of life.
A Novel Treatment for Triple-negative Breast Cancer: NS1643
Triple Negative Breast Cancer (TNBC) remains a significant cause of mortality, with 150,000 deaths annually worldwide. To address this staggering statistic, a comprehensive literature review was undertaken to explore TNBC treatments, revealing phosphorylated caveolin-1 (Cav-1) expression as pivotal in breast cancer metastasis. Interestingly, human triple-negative breast cancer cells (MDA- 231) uniquely overexpress the K+ channel Kv11.1, providing a potential drug target not present in normal breast epithelia. Treatment of MDA-231 cells with Kv11.1 activator NS1643 induced the dephosphorylation of Cav-1 and its resultant dissociation of β-catenin, a crucial regulatory protein for assembly of cell-cell adhesion complexes, towards desmosomal proteins. This experiment aimed to test if MDA-231 cells treated with NS1643 will reduce tumor cell migration and promote contact inhibition via liberation of β- catenin and its resultant interactions with desmosomal proteins. The procedure involved treating MDA-231 cells with NS1643, conducting Western blot analysis of desmosomal proteins, and measuring electrical resistance of cell monolayers grown on gold-plated microelectrodes with an epithelial cell impedance system. Results thus far indicate NS1643 rapidly increases the expression of desmosomal proteins and monolayer resistance within 24 hrs. By uncovering a novel pharmacological approach to inhibit TNBC metastasis, this study aims to not only extend patients' lives but also enhance their overall quality of life.