High expression of RTEL1 predicates worse progression in gliomas and promotes tumorigenesis through JNK/ELK1 cascade

Abstract

Abstract Gliomas are the most common primary intracranial tumor. The maintenance of telomeres serve as an important biomarker of glioma subtypes. However, the biological role of the maintenance of telomere length gene regulator of telomere length 1 (RTEL1) in glioma remains unclear. Thus, we use quantitative RT-PCR (qRT-PCR), immunohistochemistry (IHC) and western blot to determine RTEL1 expression in a cohort of glioma patients. And the biological functions of RTEL1 in glioma cells were then examined by a series of in vitro and in vivo assays. We observed that the expression of RTEL1 is positively correlated with telomere length in glioma tissue, and serve as a poor prognostic factor in TERT wild-type patients. Functional assays demonstrate that RTEL1 plays an oncogene role in glioma cell lines. In addition, RNA sequence and microarray assays were taken to identify its downstream targets. We identified phosphorylation of JNK/ELK1 signaling might be one of the mechanisms regulated by RTEL1 in glioma cells. In conclusion, Our results suggested that RTEL1 promotes glioma tumorigenesis through JNK/ELK1 cascade and indicate that RTEL1 may be a prognostic biomarker in gliomas.