Title

Spy1: A Potential Driving Force of the Breast Cancer Stem Cell (BCSC) Population

Submitter and Co-author information

Nick Philbin, University of WindsorFollow

Standing

Undergraduate

Type of Proposal

Oral Research Presentation

Challenges Theme

Building Viable, Healthy and Safe Communities

Faculty

Faculty of Science

Faculty Sponsor

Dr. Lisa Porter

Abstract/Description of Original Work

Breast cancer is the most commonly diagnosed cancer in women, and the tremendous heterogeneity of the disease complicates treatment. Triple Negative Breast Cancer (TNBC) occurs in 10-15% of the breast cancer diagnoses and typically has poorer outcomes than other subtypes of breast cancer. This is largely due to lack of targeted therapies and the existence of a population of cells known as breast cancer stem cells (BCSCs). BCSCs are more resistant to therapy and capable of driving patient relapse. Cell cycle mediators may play a key role in driving expansion of this population of dangerous cells. Spy1, a cyclin-like protein, promotes cell cycle progression through the G1/S, and the G2/M phase of the cell cycle and has been shown to be elevated in TNBC patients. Additionally, Spy1 is known to expand the brain tumour initiating cell population in brain cancers. Using an in vitromodel of the TNBC (MDA-MB-231 cell line), the relative abundancy of the BCSC population can be assessed to determine if increased levels of Spy1 can expand the BCSC population resulting in more aggressive, invasive and fatal cancers. BCSCs can be identified using markers such as the CD44 high/CD24 low, CD133 and ALDH isoforms. This work seeks to determine if Spy1 is capable of regulating the BCSC population and may allow for a potential targeted therapy to increase the survival rate of those diagnosed with TNBC.

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Spy1: A Potential Driving Force of the Breast Cancer Stem Cell (BCSC) Population

Breast cancer is the most commonly diagnosed cancer in women, and the tremendous heterogeneity of the disease complicates treatment. Triple Negative Breast Cancer (TNBC) occurs in 10-15% of the breast cancer diagnoses and typically has poorer outcomes than other subtypes of breast cancer. This is largely due to lack of targeted therapies and the existence of a population of cells known as breast cancer stem cells (BCSCs). BCSCs are more resistant to therapy and capable of driving patient relapse. Cell cycle mediators may play a key role in driving expansion of this population of dangerous cells. Spy1, a cyclin-like protein, promotes cell cycle progression through the G1/S, and the G2/M phase of the cell cycle and has been shown to be elevated in TNBC patients. Additionally, Spy1 is known to expand the brain tumour initiating cell population in brain cancers. Using an in vitromodel of the TNBC (MDA-MB-231 cell line), the relative abundancy of the BCSC population can be assessed to determine if increased levels of Spy1 can expand the BCSC population resulting in more aggressive, invasive and fatal cancers. BCSCs can be identified using markers such as the CD44 high/CD24 low, CD133 and ALDH isoforms. This work seeks to determine if Spy1 is capable of regulating the BCSC population and may allow for a potential targeted therapy to increase the survival rate of those diagnosed with TNBC.