Presenter Information

Jaymond KellyFollow

Student Major/Year in School

Biology, Third year

Faculty Mentor Information

Dr. Sherry Fleming, Biology, College of Arts and Sciences

Abstract

Blockade of B2 –GPI decreases hypoxic tissue damage

Jaymond D Kelly, Noel Nieto, Anneliese Spence, Dr. Sherry D Fleming

Division of Biology, College of Arts and Sciences

Melanoma is a deadly form of skin cancer that develops in melanocytes, which are skin cells that control pigmentation. Growing melanoma tumors become hypoxic due to outgrowing their blood vessels and lacking oxygen. In other models of hypoxia, the immune system plays a role, in particularly C3 & IgM. C3 complement activation is a part of complement cascade that begins inflammation. It is central to complement activation when the antibody, IgM is present. IgM activates the classical complement pathway and is one of the isotypes in the initial antigen-antibody complexes. As C3 and IgM are critical to hypoxia, it is likely that both C3 and IgM play a role in melanoma. B2 –glycoprotein I (B2 –GPI) is a protein in high concentration in the blood that binds to hypoxic melanoma tumors. We hypothesized that B2 –GPI plays a role in tumor growth and that blocking B2 –GPI and subsequently C3 and IgM may decrease tumor growth. We investigated melanoma tumors by injecting B16F10 cells into mice and studied them over a span of ten days while injecting peptides on multiple days. Melanoma tumors were stained for B2 –GPI, C3, and IgM binding by immunohistochemistry. We found significant B2 –GPI, C3, IgM expression in the melanoma mouse tumors. Importantly, peptides that block binding B2-GPI decreased tumor size and also decreased the staining of the tumors. Using a in vivo model, our results suggest that blocking B2 –GPI with peptides will reduce melanoma tumor growth and the peptides may be possible therapeutics for treating melanoma cancer.

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Blockade of B2 –GPI decreases hypoxic tissue damage

Blockade of B2 –GPI decreases hypoxic tissue damage

Jaymond D Kelly, Noel Nieto, Anneliese Spence, Dr. Sherry D Fleming

Division of Biology, College of Arts and Sciences

Melanoma is a deadly form of skin cancer that develops in melanocytes, which are skin cells that control pigmentation. Growing melanoma tumors become hypoxic due to outgrowing their blood vessels and lacking oxygen. In other models of hypoxia, the immune system plays a role, in particularly C3 & IgM. C3 complement activation is a part of complement cascade that begins inflammation. It is central to complement activation when the antibody, IgM is present. IgM activates the classical complement pathway and is one of the isotypes in the initial antigen-antibody complexes. As C3 and IgM are critical to hypoxia, it is likely that both C3 and IgM play a role in melanoma. B2 –glycoprotein I (B2 –GPI) is a protein in high concentration in the blood that binds to hypoxic melanoma tumors. We hypothesized that B2 –GPI plays a role in tumor growth and that blocking B2 –GPI and subsequently C3 and IgM may decrease tumor growth. We investigated melanoma tumors by injecting B16F10 cells into mice and studied them over a span of ten days while injecting peptides on multiple days. Melanoma tumors were stained for B2 –GPI, C3, and IgM binding by immunohistochemistry. We found significant B2 –GPI, C3, IgM expression in the melanoma mouse tumors. Importantly, peptides that block binding B2-GPI decreased tumor size and also decreased the staining of the tumors. Using a in vivo model, our results suggest that blocking B2 –GPI with peptides will reduce melanoma tumor growth and the peptides may be possible therapeutics for treating melanoma cancer.