KLF11/TMEM87B promoted the occurrence of glioma and decreased TMZ sensitivity.

Abstract

Whether KLF11 functions as a tumor promoter or inhibitor depends on the type of tumor. Our previous reports revealed the oncogenic role of KLF11 in glioma. In this study, TMEM87B was identified as a downstream gene of KLF11 through ChIP-seq assay, and the binding of KLF11 to the promoter area of TMEM87B was demonstrated using luciferase assay. KLF11 positively regulated the expression of TMEM87B mRNA and protein in glioma cell lines. Furthermore. TMEM87B was highly expressed in glioma samples, which indicated a poor prognosis in glioma patients. The elimination of TMEM87B reduced the proliferation and migration cell viability, along with the formation of tumor spheroids, while increasing TMZ sensitivity, whereas the overexpression of TMEM87B had the opposite effect. Furthermore, both the knockdown of TMEM87B and TMZ treatment could retard tumor growth in xenograft mice, and their combination significantly reduced tumor size and weight. Our findings identified the effects of the KLF11/ TMEM87B axis on glioma progression and TMZ sensitivity, which could provide new targets for glioma therapy.