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- W2331485210 abstract "BACKGROUND: For GBM treatment, in addition to the advancement of surgical procedure, uncovering the therapy-resistant mechanism is a crucial issue. To date, we have revealed the significance of epiregulin-mediated stemness induction for TMZ-resistance (Kohsaka, S., et al. Neuro-Oncol, 16, 960-970, 2014), and implication of glial-mesenchymal transition (GMT) for radiation resistance (Mahabir, R., et al., 16, 671-685, 2014). Since TCGA analysis revealed the frequent mutation in receptor tyrosine kinases (TKs) in GBM, several clinical trials for TK inhibitor (TKI) have been designed but no significantly effective protocol is established mainly due to the acquisition of resistance to TKIs. PURPOSE: To investigate the molecular machinery underlying TKI resistance, therapy-resistant KMG4 GBM cells against each EGFR, MET, and PDGFR were established and long-term profiling analysis with biological features was performed until day 0 to 150. RESULTS: Against our expectation, in spite of the usage of differential chemicals against individual TK as EGFR, MET, and PDGFR, all three TKI resistant GBM cells equally exhibited GMT feature in early stage around Day 50, but in the later stage this GMT profile transited to stemness-like profile both in vitro and in vivo. By microarray analysis of expression profiling, several genes were observed to be commonly elevated in all three TKI-resistant cells, and among them, IGFBP2 (insulin-like growth factor receptor binding protein2) was confirmed to be increased in four other GBM cell lines and several patient derived culture cells. Significance of IGFBP2 was proved by knockdown analysis in which siRNA for IGFBP2 re-sensitized the treatment efficiency in all three TKI-resistant cells. CONCLUSION: In the process of TKI-resistance, GBM exhibits profile transition from GMT to stemness, and IGFBP2-mediated signal can be a universal target to prevent acquisition of TKI resistance." @default.
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- W2331485210 date "2015-11-01" @default.
- W2331485210 modified "2023-09-23" @default.
- W2331485210 title "MTR-17MOLECULAR MACHINERY FOR AQUISITION OF TKI RESISTANCE IN GLIOBLASTOMA BY IGFBP2 THROUGH PROFILE TRANSITION FROM GMT TO STEMNESS FEATURE" @default.
- W2331485210 doi "https://doi.org/10.1093/neuonc/nov219.17" @default.
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