NIBAN2/FLII/RREB1 Axis Drives Glioma Stem Cell Malignancy via TLR3 Pathway Activation - PubMed
5 hours ago
- #metabolic reprogramming
- #glioma stem cells
- #TLR3 pathway
- NIBAN2 is highly expressed in glioma tissues and glioma stem-like cells (GSCs), correlating with poor patient prognosis.
- NIBAN2 binds to FLII, enhancing its interaction with RREB1, promoting nuclear translocation and activating the TLR3 signaling pathway.
- The NIBAN2-FLII-RREB1 complex forms a feed-forward loop, upregulating NIBAN2, CD44, and LDHA, driving metabolic reprogramming in GSCs.
- Multi-omics and metabolomic analyses confirm enhanced glycolytic flux, maintaining GSCs' metabolic homeostasis.
- Nelfinavir disrupts the NIBAN2-FLII complex, and combined with LDHA inhibitor FX11, shows synergistic anti-tumor effects in models.
- Clinical samples show co-upregulation of NIBAN2, FLII, and RREB1 in GBM, linked to SOX2, Ki-67, and poor prognosis.
- The study identifies a novel signaling-transcription-metabolism axis in GSCs, offering potential therapeutic targets.