In conclusion, we report that HOTAIRM1 is conducive to maintaining the malignant phenotype of tMSCs transformed by GSCs in the glioma microenvironment via E2F7 by binding to FUS and that the HOTAIRM1/FUS/E2F7 axis may be a potential target for glioma therapy (Figure S3). This evidence concerns the gene E2F7 and glioma.