DYNAMICS OF REST-TRF2 INTERACTIONS AND THE FATE OF NEURAL CANCER CELLS

Publikace nespadá pod Přírodovědeckou fakultu, ale pod Středoevropský technologický institut. Oficiální stránka publikace je na webu muni.cz.

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STOJASPAL Martin JANOVIČ Tomáš VEVERKA Pavel HOFR Ctirad

Druh Článek ve sborníku
Konference 15 th International Interdisciplinary Meeting on Bioanalysis
Fakulta / Pracoviště MU

Středoevropský technologický institut

Citace
Klíčová slova REST-TRF2 INTERACTIONS; NEURAL CANCER CELLS
Popis Glioblastomas (GBM) are the most frequent brain tumors in adults. No efficient treatment of GMB has been developed so far. The median maximum survival rate of glioblastoma-suffering patients is 12 months. The Repressor Element-1 Silencing Transcription factor (REST), also known as Neuron-Restrictive Silencing Factor (NRSF) is a transcriptional repressor recognized as a negative regulator of many genes, mainly neuronal. REST is usually expressed in nonneuronal tissues and stem cells, wherein it suppresses neuronal differentiation. REST is also present in differentiated neurons during the postnatal brain development and in normal aging, where it promotes neuroprotection by repressing genes involved in oxidative stress. But what makes REST so interesting? REST is crucial for self-renewal of cancer stem cell and brain tumor cells such as GBM. Shelterin protein TRF2 protects REST against proteasomal degradation, facilitates the physiological self-renewal of neural progenitor cells and the pathological uncontrolled proliferation of cancer cells. Identification of the interacting regions and following disruption of TRF2-REST interaction targets REST for proteasomal degradation. This could be the way how we can inhibit cancer stem cells and whole GLM tumor proliferation. In our initial studies we used FLIM-FRET (Fluorescence Lifetime Imaging Microscopy – Fluorescence Resonance Energy Transfer), PLA (proximity ligation assay) and pull-down assay to determine interacting regions of REST and TRF2.
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