Theses
Date of Award
Summer 2024
Document Type
Thesis
Degree Name
Master of Science (MS)
Department
Biological Sciences
First Advisor
Dr. Moira Sauane
Second Advisor
Dr. Stephen Redenti
Third Advisor
Dr. Columba De La Parra
Abstract
Interleukin 24 (IL-24) is a tumor-suppressing protein currently in clinical trials. IL-24 induces cancer-specific apoptosis by activating endoplasmic reticulum (ER) stress and mitochondria dysfunction. We have previously demonstrated that IL-24 leads to apoptosis in cancer cells by protein kinase A (PKA) activation in human breast cancer cells. To further understand the mechanism by which IL-24 induces apoptosis, I analyzed the role of glycogen synthase kinase-3 (GSK3), a highly conserved and normally active serine/threonine kinase in cancer cells and downstream target of PKA. The work reported here provides direct evidence that GSK3 was inhibited following IL-24 treatment in human prostate cancer cells. I showed that IL-24 inhibits GSK3b. I also showed that the inhibition of GSK3b is mediated through PKA and p38 MAPK activation triggered by IL-24. This study also found that IL-24 inhibits GSK3b and regulates apoptosis in human prostate cancer cells. Furthermore, the expression of a constitutively active form of GSKb abolishes the effect of IL-24 in the induction of apoptosis. These results demonstrate a previously unrecognized role of IL-24 in apoptosis mediated through cAMP/PKA/GSK3b regulation.
Recommended Citation
Lopez, Sual J. and Sauane, Moira, "INTERLEUKIN 24 INDUCES APOPTOSIS THROUGH GLYCOGEN SYNTHASE KINASE-3 BETA INACTIVATION IN PROSTATE CANCER CELLS" (2024). CUNY Academic Works.
https://academicworks.cuny.edu/le_etds/40
Included in
Biological Factors Commons, Cancer Biology Commons, Laboratory and Basic Science Research Commons, Molecular Biology Commons, Molecular Genetics Commons