Binghamton Research Days Student Presentations
VasquezJanelle.pdfDownregulation of MYC and KRAS modulates Ovarian Cancer Cell growth
Downregulation of MYC and KRAS modulates Ovarian Cancer Cell growth
Authors: Janelle Vasquez
Authors: Janelle Vasquez
Field of Study: Science, Technology, Engineering, and Math
Field of Study: Science, Technology, Engineering, and Math
Affiliation: TRiO participant (SSS, Upward Bound, etc.), McNair Scholars Program
Affiliation: TRiO participant (SSS, Upward Bound, etc.), McNair Scholars Program
Mentor: Tracy Brooks, School of Pharmacy and Pharmaceutical Sciences; Alexandra Maria Psaras, Laboratory Research Technician
Mentor: Tracy Brooks, School of Pharmacy and Pharmaceutical Sciences; Alexandra Maria Psaras, Laboratory Research Technician
Abstract
Abstract
Ovarian cancer is the fifth leading cause of cancer mortality among women. Aggressive ovarian cancer frequently has upregulation of two cancer proteins: KRAS and MYC. It is unknown if decreasing these proteins will affect ovarian cancer cell growth or modulate the efficacy of common chemotherapies. To address this gap in knowledge, we created a TET-ON/siRNA system where we could titrate the knocking down of each oncogene. We examined the effect of titrating the siRNA on oncogene expression and identified that 25 microgram/mL of tetracycline decreased the target oncogene expression. We also examined the effect of a tetracycline titration, and subsequently oncogene expression, on 2D and 3D cell growth. We found that knocking down the oncogenes modulated the cancer cell growth in a 3D, but not 2D, cancer cell model. With this information, cancer patients following certain criteria can benefit from this gene therapy to improve chemotherapy outcomes.
Ovarian cancer is the fifth leading cause of cancer mortality among women. Aggressive ovarian cancer frequently has upregulation of two cancer proteins: KRAS and MYC. It is unknown if decreasing these proteins will affect ovarian cancer cell growth or modulate the efficacy of common chemotherapies. To address this gap in knowledge, we created a TET-ON/siRNA system where we could titrate the knocking down of each oncogene. We examined the effect of titrating the siRNA on oncogene expression and identified that 25 microgram/mL of tetracycline decreased the target oncogene expression. We also examined the effect of a tetracycline titration, and subsequently oncogene expression, on 2D and 3D cell growth. We found that knocking down the oncogenes modulated the cancer cell growth in a 3D, but not 2D, cancer cell model. With this information, cancer patients following certain criteria can benefit from this gene therapy to improve chemotherapy outcomes.