TNFα/Grnd mediate JNK/MMPs activation during glioma progression and neurodegeneration

摘要: Glioblastoma (GB) is a type of brain tumour that involves the transformation glial cells. This most aggressive and lethal central nervous system currently there are not efficient treatments. In GB, cells display network membrane projections (cytonemes) which mediate cell to communication. Under pathological conditions like cytonemes transform into ultra-long microtubes (TMs) infiltrate brain, enwrap neurons deplete wingless (Wg)/WNT from neighbouring healthy tissue. GB establish positive feedback loop including Wg signalling, JNK matrix metalloproteases (MMP) required for progression neuronal synapse loss degeneration. Frizzled1 receptor mediates signalling upregulation activation in GB. Consequently, MMPs upregulated facilitate TMs infiltration hence expands further depletion close loop. Thus, cellular signals other than primary mutations emerge as feature correlates with poor prognosis patients animal models. Here we describe molecular mechanisms regulate production, maintenance, Drosophila model The contribution bi-directional between tissue (neurons) cells, disease. pathway mediated by Grindelwald (Grnd) activated ligand Eiger (Egr)/TNFα secreted surrounding Then, TM dissemination. show coordination among different contribute complexity versatility these incurable tumours.