Abstract
The purpose of this study is to elucidate the roles and potential underlying mechanisms of long noncoding RNA lnc-ZNF281 in glioma. We performed qRT-PCR to detect the expression levels of lnc-ZNF281 in glioma tissues. The effects of lnc-ZNF281 on the proliferative and migrative abilities of T98G and HS683 glioma cells were examined by cell proliferation assay, colony formation assay, wound-healing assay, and transwell assay. Also, the effects of lnc-ZNF281 on AKT/GSK-3β/β-catenin pathway were analyzed. The results showed that the expression of lnc-ZNF281 in glioma tissues was decreased compared with normal tissues. lnc-ZNF281 overexpression inhibited the proliferative and migrative abilities of glioma cells, while lnc-ZNF281 knockdown obtained the opposite findings. Besides, overexpression of lnc-ZNF281 in glioma cells inactivated the AKT/GSK-3β/β-catenin signaling pathway. Furthermore, β-catenin activation reversed the suppressive effects of lnc-ZNF281 on glioma cells. Taken together, lnc-ZNF281 inhibits glioma cell proliferation and migration via AKT/GSK-3β/β-catenin pathway and may serve as a potential target for glioma treatment.
Highlights
Glioma is one of the most prevalent and fatal brain tumors with low 5-year survival, approximately 5% [1]
Expression Level of lnc-ZNF281 Was Decreased in Glioma Tissues
The results showed that lnc-ZNF281 was lowly expressed in glioma tissues compared with normal brain tissues (Figure 1(a))
Summary
Glioma is one of the most prevalent and fatal brain tumors with low 5-year survival, approximately 5% [1]. Maximal resection followed by chemoradiotherapy is the currently standard treatment for glioma [2]. Immunotherapy to PD-1 and CTLA-4 exhibits promising results in glioma [3, 4]. The advances in glioma treatment really increase the survival of glioma patients, but with a high rate of recurrence and poor prognosis [2, 5]. The underlying mechanisms of highly invasive growth of glioma are unclear, and the approaches to overcome this obstacle are absent. It is imperative to explore the underlying molecular mechanisms of glioma occurrence and progression to find more effective targets for glioma treatment
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