Effects of Cannabidiol on Glioblastoma Cells

Presenter Information

Sashank Bikkasani

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Mentor Information

Dr. Subhra Mohapatra

Description

Glioblastoma is a fast-growing cancer with a mere 6.9% survival rate in patients over 5 years. New treatments are constantly being studied, but Cannabidiol (CBD) remains one of the drugs with anti-cancer properties whose pathway remains ambiguous. CBD has over 75 known protein targets, each potentially leading to a disparate cellular response. We used two glioblastoma cell lines, U251 and U87, to test the effects of CBD. U251 expresses PDGFR, EDGFR, mutant p53, and mutant TERT, while U87 expresses mutant CDKN2a, wildtype p53 and mutant PTEN, which could explain the differences in their responses to CBD treatment. This study aims to determine whether CBD is effective in treating Glioblastoma, and if it could be synergistic with other treatments, determining its mechanism of action in the two cell lines. The first part of the experiment involves the establishment of CBD’s potency in the glioblastoma cells. Cell viability assays were performed to characterize the dose-response to CBD yielding an IC50 value of 20uM in U251 cells and a 5uM in U87 cells. We used qPCR to investigate changes in CBD target genes. We found changes in genes that regulate DNA damage, oxidative stress, and inflammation pathways. In the future, we want to combine CBD with other drugs to synergistically target those pathways for a more effective treatment. We may be able to use this data to model certain drugs similar to CBD, or even find which treatments work best in synergy with CBD using its known mechanism with other complementary ones.

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Effects of Cannabidiol on Glioblastoma Cells

Glioblastoma is a fast-growing cancer with a mere 6.9% survival rate in patients over 5 years. New treatments are constantly being studied, but Cannabidiol (CBD) remains one of the drugs with anti-cancer properties whose pathway remains ambiguous. CBD has over 75 known protein targets, each potentially leading to a disparate cellular response. We used two glioblastoma cell lines, U251 and U87, to test the effects of CBD. U251 expresses PDGFR, EDGFR, mutant p53, and mutant TERT, while U87 expresses mutant CDKN2a, wildtype p53 and mutant PTEN, which could explain the differences in their responses to CBD treatment. This study aims to determine whether CBD is effective in treating Glioblastoma, and if it could be synergistic with other treatments, determining its mechanism of action in the two cell lines. The first part of the experiment involves the establishment of CBD’s potency in the glioblastoma cells. Cell viability assays were performed to characterize the dose-response to CBD yielding an IC50 value of 20uM in U251 cells and a 5uM in U87 cells. We used qPCR to investigate changes in CBD target genes. We found changes in genes that regulate DNA damage, oxidative stress, and inflammation pathways. In the future, we want to combine CBD with other drugs to synergistically target those pathways for a more effective treatment. We may be able to use this data to model certain drugs similar to CBD, or even find which treatments work best in synergy with CBD using its known mechanism with other complementary ones.