The Role of SPY1 in Mammary Involution and Oncogenesis
Standing
Graduate (Masters)
Type of Proposal
Oral Research Presentation
Faculty
Faculty of Science
Faculty Sponsor
Dr. Lisa Porter
Proposal
From puberty to menopause, factors attributed with breast cancer fluctuate with the natural mammary development. A period of increased breast cancer risk with increased metastasis and mortality occurs following childbirth – potentially linked to mammary involution: gland remodeling post lactation, which balances high rates of apoptosis and cell regeneration. Two processes controlled by the cell cycle and its regulators. The cyclin-like protein Spy1 can enable cell proliferation and override apoptosis. Spy1 levels have been found to be elevated breast cancer. Interestingly, levels of Spy1 are also elevated during involution. We hypothesized that Spy1 protects the cell population necessary for normal mammary gland reconstitution post involution. To address this, an in vitro mock involution model was deployed with the murine epithelial cell line (HC11) over a delivery and withdrawal of hormonal time course. This was paired with in vivo tissue collection of the mouse model overexpressing Spy1 in the mammary gland (MMTV-Spy1) over an involution time course. In vitro results suggest the ability of Spy1 of maintaining stemness post-differentiation, and in vivo data indicates failure of healthy epithelial clearing during involution. This research begins to articulate the role of Spy1 during normal mammary involution in maintaining the survival of epithelial cell populations, and how overexpression could potentially play a role in the predisposition of the breast to oncogenesis.
Availability
12pm - rest of the day for every day between March 29 to April 1 excepts for March 31st (Wednesday)
The Role of SPY1 in Mammary Involution and Oncogenesis
From puberty to menopause, factors attributed with breast cancer fluctuate with the natural mammary development. A period of increased breast cancer risk with increased metastasis and mortality occurs following childbirth – potentially linked to mammary involution: gland remodeling post lactation, which balances high rates of apoptosis and cell regeneration. Two processes controlled by the cell cycle and its regulators. The cyclin-like protein Spy1 can enable cell proliferation and override apoptosis. Spy1 levels have been found to be elevated breast cancer. Interestingly, levels of Spy1 are also elevated during involution. We hypothesized that Spy1 protects the cell population necessary for normal mammary gland reconstitution post involution. To address this, an in vitro mock involution model was deployed with the murine epithelial cell line (HC11) over a delivery and withdrawal of hormonal time course. This was paired with in vivo tissue collection of the mouse model overexpressing Spy1 in the mammary gland (MMTV-Spy1) over an involution time course. In vitro results suggest the ability of Spy1 of maintaining stemness post-differentiation, and in vivo data indicates failure of healthy epithelial clearing during involution. This research begins to articulate the role of Spy1 during normal mammary involution in maintaining the survival of epithelial cell populations, and how overexpression could potentially play a role in the predisposition of the breast to oncogenesis.