Fig. 8
From: Fstl1/DIP2A/MGMT signaling pathway plays important roles in temozolomide resistance in glioblastoma
The relationship among Fstl1, DIP2A, and MGMT in clinical samples. a The correlation between MGMT and Fstl1 in all GBM specimens from TCGA database (n = 165). b The correlation between MGMT and Fstl1 in GBM specimens without MGMT promoter methylation from TCGA database (n = 132). c Nineteen GBM clinical samples with MGMT promoter hypomethylation (MGMT methylation ≤ 13%) were selected for analyzing the protein levels of Fstl1, DIP2A, and MGMT in the cytoplasm or nucleus by WB. GAPDH and histone H3 were used as loading control for cytoplasm and nucleus protein, respectively. d The relationship among MGMT (NE), Fstl1 (CE), and DIP2A (NE). e The correlation among Fstl1 (CE), DIP2A (CE), and DIP2A (NE). CE cytoplasmic extracts, NE nuclear extracts. f The diagram summarizes our findings. a DIP2A interacts with DMAP1/HDAC2 to form a chromatin-modifying complex that binds within the promoter of MGMT, prevents p300 binding to the MGMT promoter region, and inhibits MGMT transcription via promoting H3K9Ac deacetylation. b Overexpression of Fstl1 arrested DIP2A in the cytoplasm and impaired the interaction between DIP2A and the DMAP1/HDAC2 repressive transcription complex, enhanced MGMT expression, and promotes temozolomide resistance
