Abstract
The long non-coding RNA Colorectal neoplasia differentially expressed (CRNDE) is a novel gene that activated early in colorectal neoplasia, but it is also up-regulated in many other solid tumors. Herein, the function and underlying mechanism of CRNDE in regulating glioma stem cells (GSCs) were investigated. We found that CRNDE expression was up-regulated while miR-186 expression was down-regulated in GSCs. Overexpression of CRNDE could promote the cellular proliferation, migration, invasion and inhibit the apoptosis in GSCs. Overexpression of miR-186 exerted functions of inhibiting the proliferation, migration and invasion of GSCs and promoting apoptosis. And CRNDE decreased the expression levels of XIAP and PAK7 by binding to miR-186 and negatively regulating it. In addition, miR-186 binded to XIAP and PAK7 3'UTR region, and decrease the expression of them, thus regulating the expression levels of downstream target proteins such as caspase 3, BAD, cyclin D1 and MARK2. The in vivo effect of CRNDE and miR-186 showed that the tumor formation rate was minimum in tumor-bearing nude mice with the knockdown of CRNDE and the overexpression of miR-186. In conclusion, CRNDE played an oncogenic role of GSCs through the negative regulation of miR-186. Both CRNDE and miR-186 could be regarded as potential targets in the glioma therapy.
Highlights
Glioma is the most prevalent primary malignant tumor in the adult human central nervous system (CNS), which is characterized by difficulty in early diagnosis and extremely poor prognosis
Colorectal neoplasia differentially expressed (CRNDE) was highly expressed in Glioma stem cells (GSCs) while miR-186 was lowly expressed in glioma tissue and GSCs
MiR-186 expression in glioma tissues was significantly decreased compared with the normal brain tissue (NBTs) and the expression was negatively correlated with the increasing pathological grades of glioma (Figure 1B)
Summary
Glioma is the most prevalent primary malignant tumor in the adult human central nervous system (CNS), which is characterized by difficulty in early diagnosis and extremely poor prognosis. Patients with glioblastoma account for 50% of new cases of malignant CNS tumors every year, and the median survival period is 0.5~1 year [1]. Glioma stem cells (GSCs) are a subgroup of glioma cells with the potentials of self-renewal, angiogenesis promotion and multi-differentiation. They are highly involved in the growth, metastasis, invasion and recurrence of glioma [2]. It’s necessary to find an effective way to control GCSs in the genetic therapy against gliomas
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