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The proposed model for the role of TRPM7-mediated HOTAIR/miR-301a-3p/FOSL1 axis in glioma tumorigenesis. TRPM7 mediates the Ca2+ influx necessary for NF-κB activation, which transcriptionally activates lncHOTAIR. In turn, lncHOTAIR directly inhibits miR-301a-3p expression, which directly functionally impede FOSL1 gene expression activity.
