Alphons Sony
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Alphons Sony has a total of 8 co-authors. Here are the top co-authors by number of shared publications:
- Anastassiya Kim
Biology Doctoral Program, The Graduate School and University Center, City University of New York New York New York USA
2 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 - Elouise Torruella
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 - Jennifer Abreu
Department of Biological Sciences, Herbert H. Lehman College, City University of New York, 250 Bedford Park Boulevard West, New York, NY 10468, USA
1 shared publication
Latest Publications
- Open Access
Inhibitory Effect of Interleukin-24 on Programmed Death Ligand 1 Expression via a Eukaryotic Translation Initiation Factor 2 Alpha Kinase 2-Dependent Pathway in Human Triple-Negative Breast Cancer
Background/Objectives: Programmed death ligand 1 (PD-L1) is often overexpressed in triple-negative breast cancer (TNBC), where it helps the tumor evade the immune system and promotes tumor growth. Interleukin-24 (IL-24) is recognized for its anti-tumor activity, although its role in immune regulation remains unclear. In this study, we examined the role of IL-24 in regulating PD-L1 and its anti-cancer activity in TNBC cells. Methods: The study used TNBC cell lines treated with IL-24, delivered via a non-replicating adenovirus vector expressing the IL-24 gene. Assays included MTT for cell viability, Annexin V for apoptosis, Western blot for protein analysis, and qRT-PCR for mRNA analysis. Results: We found that the highly aggressive MDA-MB-231 cells had significantly higher PD-L1 levels. We discovered that treatment with IL-24 reduced cell growth, induced apoptosis, and significantly decreased PD-L1 protein levels in MDA-MB-231 cells. Mechanistically, we identified PKR, also known as eukaryotic translation initiation factor 2 alpha kinase 2, as a key mediator of IL-24–induced PD-L1 suppression. Additionally, doxorubicin, a primary chemotherapy drug used to treat triple-negative breast cancer, decreases PD-L1 expression and increases the sensitivity when combined with IL-24. Conclusions: In this study, we show that IL-24 decreases PD-L1 expression in MDA-MB-231 cells through PKR activation, enhances the anti-tumor effects of Doxorubicin, and may enable lower doses that reduce toxicity and further decrease PD-L1 levels. These findings suggest that IL-24 could serve as a valuable target for therapeutic intervention and suggest that it can improve doxorubicin’s effectiveness against aggressive breast cancer.
Open AccessInhibitory Effect of Interleukin-24 on Programmed Death Ligand 1 Expression via a Eukaryotic Translation Initiation Factor 2 Alpha Kinase 2-Dependent Pathway in Human Triple-Negative Breast Cancer
Background/Objectives: Programmed death ligand 1 (PD-L1) is often overexpressed in triple-negative breast cancer (TNBC), where it helps the tumor evade the immune system and promotes tumor growth. Interleukin-24 (IL-24) is recognized for its anti-tumor activity, although its role in immune regulation remains unclear. In this study, we examined the role of IL-24 in regulating PD-L1 and its anti-cancer activity in TNBC cells. Methods: The study used TNBC cell lines treated with IL-24, delivered via a non-replicating adenovirus vector expressing the IL-24 gene. Assays included MTT for cell viability, Annexin V for apoptosis, Western blot for protein analysis, and qRT-PCR for mRNA analysis. Results: We found that the highly aggressive MDA-MB-231 cells had significantly higher PD-L1 levels. We discovered that treatment with IL-24 reduced cell growth, induced apoptosis, and significantly decreased PD-L1 protein levels in MDA-MB-231 cells. Mechanistically, we identified PKR, also known as eukaryotic translation initiation factor 2 alpha kinase 2, as a key mediator of IL-24–induced PD-L1 suppression. Additionally, doxorubicin, a primary chemotherapy drug used to treat triple-negative breast cancer, decreases PD-L1 expression and increases the sensitivity when combined with IL-24. Conclusions: In this study, we show that IL-24 decreases PD-L1 expression in MDA-MB-231 cells through PKR activation, enhances the anti-tumor effects of Doxorubicin, and may enable lower doses that reduce toxicity and further decrease PD-L1 levels. These findings suggest that IL-24 could serve as a valuable target for therapeutic intervention and suggest that it can improve doxorubicin’s effectiveness against aggressive breast cancer.
- 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.