Abstract

Long noncoding RNAs have recently been proven to regulate tumorgenesis in many cancers. However, their biological functions in glioblastoma remain largely unknown. Here we found an uncharacteristic lncRNA lncHERG that is highly expressed in human glioblastoma (GBM). We found that lncHERG knockdown inhibited cell proliferation, migration and invasion in glioblastoma in vitro and in vivo. Moreover, the higher expression of lncHERG in patients with glioblastoma indicated lower survival rate and poorer prognosis. Mechanistically, we found that lncHERG can serve as a sponge for miR-940 which is a tumor suppressor in cervical cancer and whose function has not been defined in glioblastoma. We showed that miR-940 was down-regulated in glioblastoma tissues compared to peritumor tissues. LncHERG knockdown impaired cell proliferation, migration and invasion while inhibition of miR-940 in the meantime reversed this trend. In conclusion, our study highlights the essential role of lncHERG in glioblastoma by acting as a competing endogenous RNA of miR-940, which may serve as a new prognostic biomarker in glioblastoma.

Highlights

  • Glioblastoma (GBM), the most common and aggressive brain tumor around the world, leads to a large amount of deaths each year [1, 2]

  • Our study highlights the essential role of lncHERG in glioblastoma by acting as a competing endogenous RNA of miR-940, which may serve as a new prognostic biomarker in glioblastoma

  • We showed that lncHERG depletion impaired proliferation, migration and invasion of glioblastoma in vitro and in vivo

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Summary

Introduction

Glioblastoma (GBM), the most common and aggressive brain tumor around the world, leads to a large amount of deaths each year [1, 2]. Radiotherapy and chemotherapy were the main methods for treatment of GBM patients [3,4,5,6]. The 5-year overall survival rate of patients with GBM is less than 3% [7, 8]. Due to the infiltrative growth of glioblastoma, the rate of tumor recurrence is very high [5]. There is no effective method for fully treatment of glioblastoma so far. In order to develop new and effective therapeutic management of GBM, it is an urgent and necessary to define the molecular mechanism that regulates the genesis of glioblastoma

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