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shRNA-MCT2 is an experimental RNA interference-based therapeutic tool designed to silence the expression of Monocarboxylate Transporter 2 (MCT2), a protein encoded by the SLC16A7 gene. MCT2 is primarily responsible for the high-affinity uptake of monocarboxylates, such as lactate and pyruvate, into cells, particularly neurons. In the context of glioblastoma, research indicates that a metabolic coupling exists where residual tumor cells utilize lactate provided by the microenvironment to fuel regrowth and invasion after surgical resection. shRNA-MCT2 is typically delivered via a viral vector, such as recombinant adeno-associated virus (rAAV), often under the control of a neuron-specific promoter like human synapsin (hSyn). By knocking down MCT2, the treatment disrupts this lactate-fueled metabolic axis, thereby reducing tumor proliferation, invasive growth, and the formation of tumor-neuron synaptic contacts. This approach targets the narrow window of metabolic adaptation that occurs immediately following surgical intervention to prevent local tumor relapse.
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