Life Sciences Seminar: Targeting NFkB May Overcome VSV Resistance in Prostate Cancer
Life Sciences Seminar
Targeting NFkB May Overcome VSV Resistance in Prostate Cancer
Dr. Maureen Ferran
Professor, School of Life Sciences
Rochester Institute of Technology
Abstract: Vesicular stomatitis virus (VSV) is being studied as an oncolytic, or cancer-killing, virus because it can selectively destroy tumor cells while leaving normal cells unharmed. However, some aggressive cancer cells are resistant to VSV-induced killing. The goal of our research is to understand the molecular mechanisms behind this resistance. We found that highly metastatic prostate cancer cells (such as PC3) strongly activate a signaling pathway called NFkB following VSV infection. This activation increases the expression of genes that block cell death and inhibit viral replication, allowing the cancer cells to survive. In contrast, NFkB is not activated in less aggressive prostate cancer cells that are easily killed by the virus. Importantly, when we inhibit NFkB or block one of its target proteins, BCL-2, the resistant cells become sensitive to VSV again. These findings reveal that NFkB plays a key role in helping prostate cancer cells evade oncolytic virus killing and point to new strategies to enhance the effectiveness of VSV-based cancer therapies.
Intended Audience: Beginners, undergraduates, graduates. Those with interest in the topic.
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