MCF-7 Dense Breast Cancer Cells Modulate Stress Through Senescence
Molloy Faculty Mentor
Noelle Cutter
Presenter Major
Biology
Presentation Type
Poster
Location
H239, 2nd floor, Barbara H. Hagan Center for Nursing
Start Date
28-4-2025 5:55 PM
End Date
28-4-2025 6:55 PM
Description (Abstract)
Breast cancer remains a leading cause of cancer-related mortality among women worldwide, with dense breast tissue being recognized as a significant risk factor for its development. This dense breast tissue, characterized by a higher concentration of mammary glandular tissue, represents additional sites for tumor development. The following study explores how the MCF-7 immortal cell line, representing dense breast cancer, modulates stress responses through cellular senescence. Cellular senescence is a defense mechanism that halts the cell cycle and acts as a tumor suppression mechanism, preventing out-of-control cell proliferation triggered by cytological stress. To simulate these stress conditions, we applied two agents: carboplatin (CBDCA), a platinoid chemotherapeutic medicine that alters the structure of DNA and has downstream effects on a cell’s ability to replicate said DNA; and hydrogen peroxide (H2O2), a common cytological stress indicator which itself can also act as a stressor under high enough concentration and exposure times. This study measured cell proliferation and activity, cytological stress responses, and the senescence response of MCF-7 and Br(EPI) cell lines to the introduced stressors. The results demonstrated that MCF-7 cells exhibited vastly increased cytological stress resistance and proliferation than non-tumorigenic cells. When exposed to CBDCA, the MCF-7 cell lines did not undergo apoptosis characterized by Caspase-3 activation. Instead, they entered a state of cellular senescence, allowing the cells to adapt and continue proliferation. These findings highlighted critical cellular mechanisms in dense breast cancer, suggesting potential targets for future research. Furthermore, the study underscores the role of cellular senescence in the promotion of metastasis of breast cancer by making the tumor environment more favorable to angiogenesis, immune evasion, and tumor progression. Further research into the specific hormonal, physiological, and cytological changes in dense breast tumor environments may present novel, personalized treatment methods to improve patient outcomes.
Keywords
Breast Cancer, Oncology, Cytotoxicity, Chemotherapy, Senescence, Dense Breast Tissue
Related Pillar(s)
Study
MCF-7 Dense Breast Cancer Cells Modulate Stress Through Senescence
H239, 2nd floor, Barbara H. Hagan Center for Nursing
Breast cancer remains a leading cause of cancer-related mortality among women worldwide, with dense breast tissue being recognized as a significant risk factor for its development. This dense breast tissue, characterized by a higher concentration of mammary glandular tissue, represents additional sites for tumor development. The following study explores how the MCF-7 immortal cell line, representing dense breast cancer, modulates stress responses through cellular senescence. Cellular senescence is a defense mechanism that halts the cell cycle and acts as a tumor suppression mechanism, preventing out-of-control cell proliferation triggered by cytological stress. To simulate these stress conditions, we applied two agents: carboplatin (CBDCA), a platinoid chemotherapeutic medicine that alters the structure of DNA and has downstream effects on a cell’s ability to replicate said DNA; and hydrogen peroxide (H2O2), a common cytological stress indicator which itself can also act as a stressor under high enough concentration and exposure times. This study measured cell proliferation and activity, cytological stress responses, and the senescence response of MCF-7 and Br(EPI) cell lines to the introduced stressors. The results demonstrated that MCF-7 cells exhibited vastly increased cytological stress resistance and proliferation than non-tumorigenic cells. When exposed to CBDCA, the MCF-7 cell lines did not undergo apoptosis characterized by Caspase-3 activation. Instead, they entered a state of cellular senescence, allowing the cells to adapt and continue proliferation. These findings highlighted critical cellular mechanisms in dense breast cancer, suggesting potential targets for future research. Furthermore, the study underscores the role of cellular senescence in the promotion of metastasis of breast cancer by making the tumor environment more favorable to angiogenesis, immune evasion, and tumor progression. Further research into the specific hormonal, physiological, and cytological changes in dense breast tumor environments may present novel, personalized treatment methods to improve patient outcomes.
