Effects of AG490 and Stattic on MDA-MB-453 breast carcinoma cells and c-SRC
Location
Room 232, Schewel Hall
Access Type
Open Access
Entry Number
81
Start Date
4-5-2023 9:45 AM
End Date
4-5-2023 10:00 AM
College
Lynchburg College of Arts and Sciences
Department
Biomedical Science
Abstract
Breast cancer is a complex disease that progresses through the aberrant activation of cell signaling pathways.This study analyzes the JAK/STAT pathway, a pathway that can become atypically activated in breast cancer cells leading to tumor progression and proliferation. The JAK/STAT pathway in normal cells is involved in cell proliferation, differentiation, cell migration, and apoptosis. This pathway is a great model for studying cancer's proliferative properties through the use of inhibitors that target the JAK/STAT pathway. c-SRC is a protein that presents itself in higher amounts in breast cancer cells. Evidence shows that c-SRC plays a key role in cancer proliferation by interacting with a number of cell pathways such as the JAK/STAT pathway. In this study, we tested two inhibitors on MDA-MB-453 breast carcinoma cells: AG490, a JAK-specific inhibitor, and stattic, a STAT-specific inhibitor. These inhibitors are known to target and inhibit the activation of the JAK/STAT pathway. We studied the effects of each drug on cell survival, at varying doses and exposure times. Preliminary data suggests that breast cancer cell exposure to 100 µM AG490 at 48 hours contributes to cell death. Preliminary data also suggests that 20 µM stattic at 48 and 72 hours contributes to cell death. Analyzing the presence of c-SRC and its activity during breast cancer cell exposure to 100 µM of AG490 at 48 hours will provide us with a better idea of its role in breast cancer cell growth.
Faculty Mentor(s)
Dr. Allison Jablonski
Rights Statement
The right to download or print any portion of this material is granted by the copyright owner only for personal or educational use. The author/creator retains all proprietary rights, including copyright ownership. Any editing, other reproduction or other use of this material by any means requires the express written permission of the copyright owner. Except as provided above, or for any other use that is allowed by fair use (Title 17, §107 U.S.C.), you may not reproduce, republish, post, transmit or distribute any material from this web site in any physical or digital form without the permission of the copyright owner of the material.
Harrison SSS
Effects of AG490 and Stattic on MDA-MB-453 breast carcinoma cells and c-SRC
Room 232, Schewel Hall
Breast cancer is a complex disease that progresses through the aberrant activation of cell signaling pathways.This study analyzes the JAK/STAT pathway, a pathway that can become atypically activated in breast cancer cells leading to tumor progression and proliferation. The JAK/STAT pathway in normal cells is involved in cell proliferation, differentiation, cell migration, and apoptosis. This pathway is a great model for studying cancer's proliferative properties through the use of inhibitors that target the JAK/STAT pathway. c-SRC is a protein that presents itself in higher amounts in breast cancer cells. Evidence shows that c-SRC plays a key role in cancer proliferation by interacting with a number of cell pathways such as the JAK/STAT pathway. In this study, we tested two inhibitors on MDA-MB-453 breast carcinoma cells: AG490, a JAK-specific inhibitor, and stattic, a STAT-specific inhibitor. These inhibitors are known to target and inhibit the activation of the JAK/STAT pathway. We studied the effects of each drug on cell survival, at varying doses and exposure times. Preliminary data suggests that breast cancer cell exposure to 100 µM AG490 at 48 hours contributes to cell death. Preliminary data also suggests that 20 µM stattic at 48 and 72 hours contributes to cell death. Analyzing the presence of c-SRC and its activity during breast cancer cell exposure to 100 µM of AG490 at 48 hours will provide us with a better idea of its role in breast cancer cell growth.