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Enhanced CpG Activated Macrophage Killing of 3-Bromopyruvate Pre-treated 4T1 Breast Cancer Cells
Title
Enhanced CpG Activated Macrophage Killing of 3-Bromopyruvate Pre-treated 4T1 Breast Cancer Cells.
Creator
Rumicha, Dawit, Liddle, Genevieve M., Hartmann, James X., Office of Undergraduate Research and Inquiry
Abstract/Description
A common feature of breast cancer cells is the evasion of singular treatments by using the Warburg Effect, a process of metabolic ATP production through rapid anaerobic glycolysis. Cancer research has transitioned to an investigation of combination therapies to combat cancer. In our study, we seek to metabolically inhibit cancer cells before application of immunogenic killing. The Warburg Effect was targeted with 3-Bromopyruvate (3-BP), which blocks Glyceraldehyde 3-Phosphate Dehydrogenase ...
Show moreA common feature of breast cancer cells is the evasion of singular treatments by using the Warburg Effect, a process of metabolic ATP production through rapid anaerobic glycolysis. Cancer research has transitioned to an investigation of combination therapies to combat cancer. In our study, we seek to metabolically inhibit cancer cells before application of immunogenic killing. The Warburg Effect was targeted with 3-Bromopyruvate (3-BP), which blocks Glyceraldehyde 3-Phosphate Dehydrogenase (GAPDH) production. Treatment with 3-BP yielded up to 86.5% cancer cell death. Glycolytic inhibition renders cancer cells metabolically stressed, which may enable an effective immune response. Our hypothesis was that CpG activated macrophage will possess tumoricidal potential to target metabolically stressed cancer cells. Macrophages and CpG cultivation alone yielded a significant immune response. We sought to find a synergistic effect of 3-BP induced killing susceptibility with CpG activated macrophages may lead to an effective method of combination therapy.
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Date Issued
2017
PURL
http://purl.flvc.org/fau/fd/FA00005634
Subject Headings
College students --Research --United States.
Format
Document (PDF)
A Study on Reversing the Immunosuppressive Phenotype of Tumor Associated Macrophages
Title
A Study on Reversing the Immunosuppressive Phenotype of Tumor Associated Macrophages.
Creator
Liddle, Genevieve M., Hartmann, James X., Florida Atlantic University, Charles E. Schmidt College of Science, Department of Biological Sciences
Abstract/Description
Extracellular stimuli may influence the M1/M2 phenotypic polarization of macrophages. We examined M1/M2 biomarkers, phagocytic activity, and tumoricidal activity in RAW 264.7 mouse macrophages. Macrophages were treated with conditioned media (CM) from 4T1 breast cancer cells, curcumin, 22-oxacalcitriol, LPS, or a combination of the previously listed. Arginase activity, a M2 phenotypic biomarker, was upregulated by the treatment of macrophages with conditioned media. Curcumin, 22-...
Show moreExtracellular stimuli may influence the M1/M2 phenotypic polarization of macrophages. We examined M1/M2 biomarkers, phagocytic activity, and tumoricidal activity in RAW 264.7 mouse macrophages. Macrophages were treated with conditioned media (CM) from 4T1 breast cancer cells, curcumin, 22-oxacalcitriol, LPS, or a combination of the previously listed. Arginase activity, a M2 phenotypic biomarker, was upregulated by the treatment of macrophages with conditioned media. Curcumin, 22- oxacalcitriol, and LPS partially inhibited RAW 264.7 arginase activity in the presence of 4T1 breast cancer media. 22-oxacalcitriol increased the phagocytic ability of RAW 264.7 macrophages in the presence of M2 polarizing substances produced by the 4T1 breast cancer cells. Also, LPS increased RAW 264.7 phagocytic ability in the presence of 4T1 breast cancer CM. This study looked at the potential substances that would possibly reverse the M2 tumor promoting macrophage phenotype seen in the breast cancer tumor environment.
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Date Issued
2017
PURL
http://purl.flvc.org/fau/fd/FA00004867
Subject Headings
Macrophages., Breast--Cancer--Treatment., Tumors--Immunological aspects., Cancer--Immunological aspects., Biological response modifiers., Cancer--Molecular aspects.
Format
Document (PDF)