Mutated KLF4(K409Q) in meningioma binds STRs and activates FGF3 gene expression. Tsytsykova et al.
Meningiomas are the most common primary tumors of the central nervous system. The genetic landscape of the most common subtype of meningioma involves mutation or copy loss of the NF2 gene in approximately 50% of cases. Other recurrent canonical somatic mutations are present in ~40% of sporadic meningiomas and are not defined by NF2 inactivation. These genes include TRAF7, AKT1, SMO, and KLF4, among others. Tumors with KLF4 and TRAF7 mutations share a unique secretory phenotype, which is characterized by glandular lumina with secretory globules, and tend to cause disproportional peritumoral edema, which can cause severe medical and neurological complications in pre- and post-operative management. The K409Q mutation in KLF4 is found in ~15% of meningiomas. The mutated allele KLF4(K409Q) is the same in all affected patients and occurs together with TRAF7 missense mutations. The contribution of the meningioma-specific KLF4 mutation to tumorigenesis and mechanism of action is unknown. Data sets included here contain raw RNA-seq data files from high throughput sequencing, which can be used by other investigators in meta-analysis. Cells were transiently transfected with p3XFLAG-CMV™-7.1 vectors expressing KLF4 or KLF4(K409Q) proteins and kept in culture. RNA-sequencing was performed to identify differentially regulated genes upon ectopic expression of FLAG-tagged KLF4 or KLF4(K409Q) in two different cell lines, HEK293 and A549.