This summer I was able to continue researching mechanisms in cancer metabolism under Dr. Kathryn Wellen of the Department of Cancer Biology in the Perelman School of Medicine. One of the main focuses of the lab is the role of acetyl-coA in the interaction between epigenetic mechanisms and metabolic pathways for cancer cells. The project I worked on was specifically about glioblastoma cells, a highly malignant form of brain cancer. Our goal was to better understand how cancer cells utilize their altered metabolic functions to enhance growth and survival. The lab previously found that certain genes respond to the availability of acetyl-coA, an important metabolite derived mainly from glucose. This was demonstrated by the varying levels of histone acetylation to different nutrient and glucose availability. Our focus became which gene pathways were involved and regulated by acetyl-coA availability that would lead to the distinct phenotypes of glioblastoma cells. We found that many of the genes involved were also involved in migration and adhesion, means by which tumor cells can metastasize. We found that a key player within these gene pathways was the transcription factor NFAT. We wanted to understand what are the functional consequences of NFAT regulation by glucose levels in reference to the adhesion/migration phenotype of glioblastoma cells, and what are possible mechanisms by which NFAT was regulating these pathways.
This summer I was able to continue researching mechanisms in cancer metabolism under Dr. Kathryn Wellen of the Department of Cancer Biology in the Perelman School of Medicine. One of the main focuses of the lab is the role of acetyl-coA in the interaction between epigenetic mechanisms and metabolic pathways for cancer cells. The project I worked on was specifically about glioblastoma cells, a highly malignant form of brain cancer. Our goal was to better understand how cancer cells utilize their altered metabolic functions to enhance growth and survival. The lab previously found that certain genes respond to the availability of acetyl-coA, an important metabolite derived mainly from glucose. This was demonstrated by the varying levels of histone acetylation to different nutrient and glucose availability. Our focus became which gene pathways were involved and regulated by acetyl-coA availability that would lead to the distinct phenotypes of glioblastoma cells. We found that many of the genes involved were also involved in migration and adhesion, means by which tumor cells can metastasize. We found that a key player within these gene pathways was the transcription factor NFAT. We wanted to understand what are the functional consequences of NFAT regulation by glucose levels in reference to the adhesion/migration phenotype of glioblastoma cells, and what are possible mechanisms by which NFAT was regulating these pathways.