Sual Lopez
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Sual Lopez has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Columba de la Parra
Ph.D. Program in Biology, The Graduate Center, City University of New York, 365 Fifth Avenue, New York, NY 10016, USA
2 shared publications - Moira Sauane
Department of Biological Sciences, Herbert H. Lehman College, City University of New York, 250 Bedford Park Boulevard West, Bronx, NY 10468, USA
2 shared publications - Simira Smith
Department of Biological Sciences, Herbert H. Lehman College, City University of New York, 250 Bedford Park Boulevard West, Bronx, NY 10468, USA
2 shared publications - Alphons Sony
Department of Biological Sciences, Herbert H. Lehman College, City University of New York, 250 Bedford Park Boulevard West, Bronx, NY 10468, USA
1 shared publication - Anastassiya Kim
Ph.D. Program in Biology, The Graduate Center, City University of New York, 365 Fifth Avenue, New York, NY 10016, USA
1 shared publication - Anastassiya Kim
Biology Doctoral Program, The Graduate School and University Center, City University of New York New York New York USA
1 shared publication
Latest Publications
- Open Access
Interleukin 24 Promotes Mitochondrial Dysfunction, Glucose Regulation, and Apoptosis by Inactivating Glycogen Synthase Kinase 3 Beta in Human Prostate Cancer Cells
Interleukin 24 (IL-24) is a tumor-suppressing protein currently in clinical trials. We previously demonstrated that IL-24 leads to apoptosis in cancer cells through protein kinase A (PKA) activation in human breast cancer cells. To better understand the mechanism by which IL-24 induces apoptosis, we analyzed the role of glycogen synthase kinase-3 beta (GSK3β), a highly conserved serine/threonine kinase in cancer cells and a downstream target of PKA. Our studies show for the first time that GSK3β is inhibited following IL-24 treatment in human prostate cancer cells. We showed that the inhibition of GSK3β is mediated through PKA activation triggered by IL-24. IL-24 decreases the phosphorylation of glycogen synthase, substantially activating glycogen synthase and decreasing intracellular glucose levels. Notably, the expression of a constitutively active form of GSK3β abolishes the effect of IL-24. These results demonstrate a previously unrecognized role of IL-24 in apoptosis mediated through GSK3β regulation and its possible implications for metabolic stress, mitochondria dysfunction, and apoptosis. Future studies should precisely delineate the most effective combinations of IL-24 as a GSK3β inhibitor with cytotoxic agents for prostate and other cancers. GSK3β inhibition disrupts average glucose utilization in cancer cells, potentially creating metabolic stress that could be exploited therapeutically.
Open AccessInterleukin 24 Promotes Mitochondrial Dysfunction, Glucose Regulation, and Apoptosis by Inactivating Glycogen Synthase Kinase 3 Beta in Human Prostate Cancer Cells
Interleukin 24 (IL-24) is a tumor-suppressing protein currently in clinical trials. We previously demonstrated that IL-24 leads to apoptosis in cancer cells through protein kinase A (PKA) activation in human breast cancer cells. To better understand the mechanism by which IL-24 induces apoptosis, we analyzed the role of glycogen synthase kinase-3 beta (GSK3β), a highly conserved serine/threonine kinase in cancer cells and a downstream target of PKA. Our studies show for the first time that GSK3β is inhibited following IL-24 treatment in human prostate cancer cells. We showed that the inhibition of GSK3β is mediated through PKA activation triggered by IL-24. IL-24 decreases the phosphorylation of glycogen synthase, substantially activating glycogen synthase and decreasing intracellular glucose levels. Notably, the expression of a constitutively active form of GSK3β abolishes the effect of IL-24. These results demonstrate a previously unrecognized role of IL-24 in apoptosis mediated through GSK3β regulation and its possible implications for metabolic stress, mitochondria dysfunction, and apoptosis. Future studies should precisely delineate the most effective combinations of IL-24 as a GSK3β inhibitor with cytotoxic agents for prostate and other cancers. GSK3β inhibition disrupts average glucose utilization in cancer cells, potentially creating metabolic stress that could be exploited therapeutically.
- Open Access
Interleukin 24: Signal Transduction Pathways
Interleukin 24 is a member of the IL-10 family with crucial roles in antitumor, wound healing responses, host defense, immune regulation, and inflammation. Interleukin 24 is produced by both immune and nonimmune cells. Its canonical pathway relies on recognition and interaction with specific Interleukin 20 receptors in the plasma membrane and subsequent cytoplasmic Janus protein tyrosine kinases (JAK)/signal transducer and activator of the transcription (STAT) activation. The identification of noncanonical JAK/STAT-independent signaling pathways downstream of IL-24 relies on the interaction of IL-24 with protein kinase R in the cytosol, respiratory chain proteins in the inner mitochondrial membrane, and chaperones such as Sigma 1 Receptor in the endoplasmic reticulum. Numerous studies have shown that enhancing or inhibiting the expression of Interleukin 24 has a therapeutic effect in animal models and clinical trials in different pathologies. Successful drug targeting will require a deeper understanding of the downstream signaling pathways. In this review, we discuss the signaling pathway triggered by IL-24.
Open AccessInterleukin 24: Signal Transduction Pathways
Interleukin 24 is a member of the IL-10 family with crucial roles in antitumor, wound healing responses, host defense, immune regulation, and inflammation. Interleukin 24 is produced by both immune and nonimmune cells. Its canonical pathway relies on recognition and interaction with specific Interleukin 20 receptors in the plasma membrane and subsequent cytoplasmic Janus protein tyrosine kinases (JAK)/signal transducer and activator of the transcription (STAT) activation. The identification of noncanonical JAK/STAT-independent signaling pathways downstream of IL-24 relies on the interaction of IL-24 with protein kinase R in the cytosol, respiratory chain proteins in the inner mitochondrial membrane, and chaperones such as Sigma 1 Receptor in the endoplasmic reticulum. Numerous studies have shown that enhancing or inhibiting the expression of Interleukin 24 has a therapeutic effect in animal models and clinical trials in different pathologies. Successful drug targeting will require a deeper understanding of the downstream signaling pathways. In this review, we discuss the signaling pathway triggered by IL-24.