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

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Apr 5th, 9:45 AM Apr 5th, 10:00 AM

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.