Figure 3
From: KLF6 depletion promotes NF-κB signaling in glioblastoma
KLF6 induces NF-κB-negative regulators in glioblastoma. (a–c) Infection of LN229 (a), BTSC23 (b) and BTSC233 (c) cells with pCHMWS lentivirus carrying FLAG-tagged KLF6-wt or KLF6-sv1 cDNA, or empty vector (EV), captured by immunoblotting. (d– f) qRT-PCR analysis of relative transcript expression of TNIP1, TNIP2, NFKBIA and TNFAIP3 in LN229 (d), BTSC23 (e), BTSC233 (f) cells expressing EV, KLF6-wt or KLF6-sv1. (g) Immunoblotting of KLF6, TNFAIP3, NFKBIA in LN229 cells expressing EV, KLF6-wt or KLF6-sv1. (h) Schematic representation and position of KLF6 binding sites in the promoters of TNIP1, TNIP2, NFKBIA and TNFAIP3 genes. Stars indicate binding sites validated by chromatin immunoprecipitation. (i) qRT-PCR analysis showing enriched binding of KLF6 to specific promoters in LN229 cells expressing EV, KLF6-wt or KLF6-sv1. The SERPINA1 and OLR1 gene promoters were positive and negative controls, respectively. Relative gene expressions are normalized to EV, representative qRT-PCR of three independent experiments. (d– f). Error bars represent mean±s.d.
