The Office of the Vice President for Research recognizes Zhi Sheng, an assistant professor at the Virginia Tech Carilion Research Institute, where he focuses on developing new therapies for glioblastoma, a lethal and incurable brain cancer.
Sheng is also an assistant professor of biomedical sciences and pathobiology in the Virginia–Maryland College of Veterinary Medicine.
Despite a range of therapies for glioblastoma multiforme, including the symptomatic relief that can come from the surgical removal of a tumor, malignant cells invariably return, leading to a median survival time after diagnosis of just over a year.
Several factors complicate treatment: the resistance of the tumor cells to conventional therapies, the vulnerability of the brain to damage from those therapies, and the ability of the cells to evade even the most skilled surgical hand.
Sheng uses an innovative strategy for his research. He takes advantage of two intrinsic cellular processes — autophagy, the process of cellular self-digestion, and apoptosis, programmed cell death — to cause the malignant brain tumor cells to degrade and even kill themselves.
Autophagy and apoptosis are often misregulated in cancer stem cells and contribute to therapeutic resistance, so Sheng’s research takes a dual approach: characterizing the genes that regulate these processes in glioblastoma while also determining the role these processes play in both the genesis and therapeutic resistance of glioblastoma.
Sheng’s research with colleagues in Korea revealed a molecular mechanism that splices RNA and, in turn, controls the self-destruction of cells. Although the core of our genetic identity is stagnant in DNA, the expression of our genetic code can change over time, through cell replications.
The same string of genetic code can be cut at different points and in different lengths to form different segments of RNA — the middleman between DNA and the molecular machines that build proteins.
Sheng and his team found that the same gene cut at different lengths affects the cell in different ways. FAS-L, the long form, promotes cell death, while FAS-S, the short form, discourages it. The finding helps researchers understand how natural cell death is silenced in cancer cells and has implications in cancer therapeutic interventions.
Before joining the Virginia Tech Carilion Research Institute, Sheng completed a postdoctoral fellowship in the Program in Gene Function and Expression at the University of Massachusetts Medical School in Worcester, Massachusetts.
There he studied the molecular pathways regulating apoptosis and autophagy in malignant cells and the mechanisms of chronic myelogenous leukemia.
Sheng earned a bachelor’s degree in forensic science and a master’s degree in biochemistry at Shanghai Medical College of Fudan University in Shanghai, China, before earning a doctorate in molecular and cell biology at the State University of New York Downstate Medical Center in Brooklyn, New York.
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