Investigation of FX-11 Induced Oxidative Stress on Hsp90 Expression in HL60 Acute Myeloid Leukemia Cells
University
Shawnee State University
Major
Biomedical Science
Student Type
Undergraduate Student
Presentation Types
Oral Presentation (Live)
Keywords:
Leukemia, Warburg Effect, Metabolism, Hsp90
Abstract
Acute myeloid leukemia (AML) is a promyelocytic cancer characterized by uncontrolled hematopoietic progenitor cell division. AML exhibits an unusual basal metabolic phenotype called the Warburg Effect. The Warburg Effect describes cells who rely on glycolysis and fermentation to produce energy instead of utilizing the conventional mitochondrial aerobic respiration pathways. FX-11 is a lactate dehydrogenase A inhibitor that prevents cells from performing fermentation, thus forcing the cells to rely on their mitochondria to produce energy. This in turn increases reactive oxygen species (ROS). Studies have shown Hsp90, an important molecular chaperone that provides a protective function for cancer cells, is susceptible to cleavage by ROS. This study aims to examine mechanisms of FX-11 toxicity in HL60 AML cells by performing in vitro cytotoxic assays, measuring ROS species production and measuring Hsp90 levels with treatment.
Human and Animal Subjects
no
Faculty Mentor Name
Jennifer Napper
Faculty Mentor Title
Professor of Biology
Faculty Mentor Department
Natural Sciences
Recommended Citation
Johnson, Nathan, "Investigation of FX-11 Induced Oxidative Stress on Hsp90 Expression in HL60 Acute Myeloid Leukemia Cells" (2025). Celebration of Scholarship. 3.
https://digitalcommons.shawnee.edu/cos/2025/session5/3
Location
LIB 204
Investigation of FX-11 Induced Oxidative Stress on Hsp90 Expression in HL60 Acute Myeloid Leukemia Cells
LIB 204
Acute myeloid leukemia (AML) is a promyelocytic cancer characterized by uncontrolled hematopoietic progenitor cell division. AML exhibits an unusual basal metabolic phenotype called the Warburg Effect. The Warburg Effect describes cells who rely on glycolysis and fermentation to produce energy instead of utilizing the conventional mitochondrial aerobic respiration pathways. FX-11 is a lactate dehydrogenase A inhibitor that prevents cells from performing fermentation, thus forcing the cells to rely on their mitochondria to produce energy. This in turn increases reactive oxygen species (ROS). Studies have shown Hsp90, an important molecular chaperone that provides a protective function for cancer cells, is susceptible to cleavage by ROS. This study aims to examine mechanisms of FX-11 toxicity in HL60 AML cells by performing in vitro cytotoxic assays, measuring ROS species production and measuring Hsp90 levels with treatment.
