Nikhila Anand
Pronouns: she/her
Research Mentor(s): Qing Li
Co-Presenter:
Research Mentor School/College/Department: Medicine Division of Hematology & Oncology / Medicine
Presentation Date: April 20
Presentation Type: Poster
Session: Session 3 – 1:40pm – 2:30 pm
Room: League Ballroom
Authors:
Presenter: 54
Abstract
Many cancers reprogram their metabolic processes and have been found to rely more on fatty acids for fuel. However, the role of acetyl-CoA carboxylase (ACC) and its isoforms (ACC1 and ACC2) in fatty acid synthesis (FAS) during a leukemic state is not entirely understood. ACC is a key enzyme involved in the rate-limiting step of FAS, as it converts acetyl-CoA to malonyl-CoA. The purpose of this project is to test two ACC inhibitors (TOFA and PF-05175157) on four leukemia cell lines, specifically AML2, AML3, MOLM-13, and THP-1. Growth curves and sensitivities were established for these cell lines with each inhibitor by measuring cell count and viability 24, 48, and 72h post treatment. Next, with the use of antibody staining (Annexin V and DAPI) and flow cytometry, apoptosis assays were conducted to establish an optimal time point in which cells are apoptotic (Annexin V +) but not yet necrotic (DAPI-). The results of these preliminary assays show that THP-1 is the most sensitive to the PF-05175157 inhibitor compared to AML3 and MOLM-13 at the drug concentration of 100 ug/mL. Interestingly for TOFA, MOLM-13 and AML2 cells are more sensitive than AML3 and THP-1. Together these findings suggest that each cell line, each with unique mutations and conditions that are needed to proliferate, are impacted by both ACC inhibitors in different mechanisms. Future mitochondrial and protein expression assays are going to be conducted in order to uncover the underlying mechanisms of fatty acid metabolism that are necessary for leukemia cells to grow.
Interdisciplinary, Natural/Life Sciences
