Upregulation of long noncoding RNA zinc finger antisense 1 enhances epithelial–mesenchymal transition in vitro and predicts poor prognosis in glioma

Author:

Lv Qiao-Li12,Chen Shu-Hui3,Zhang Xue12,Sun Bao12,Hu Lei12,Qu Qiang4,Huang Yuan-Tao5,Wang Gui-Hua3,Liu Yan-Ling12,Zhang Ying-Ying6,Zhou Hong-Hao12

Affiliation:

1. Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, P.R. China

2. Hunan Key Laboratory of Pharmacogenetics, Institute of Clinical Pharmacology, Central South University, Changsha, P.R. China

3. Department of Oncology, Changsha Central Hospital, Changsha, P.R. China

4. Department of Pharmacy, Xiangya Hospital, Central South University, Changsha, P.R. China

5. Department of Neurology, The Brain Hospital of Hunan Province, Changsha, P.R. China

6. Department of Oncology, Xiangya Hospital, Central South University, Changsha, P.R. China

Abstract

Increasing evidence indicates that long noncoding RNAs play important roles in development and progression of various cancers. Zinc finger antisense 1 is a novel long noncoding RNA whose clinical significance, biological function, and underlying mechanism are still undetermined in glioma. In this study, we reported that zinc finger antisense 1 expression was markedly upregulated in glioma and tightly correlated with clinical stage. Moreover, patients with high zinc finger antisense 1 expression had shorter survival. Multivariate Cox regression analysis provided a clue that, probably, zinc finger antisense 1 level could serve as an independent prognostic factor for glioma. Functionally, zinc finger antisense 1 acted as an oncogene in glioma because its knockdown could promote apoptosis and significantly inhibit cell proliferation, migration, and invasion. Furthermore, zinc finger antisense 1 silencing could result in cell cycle arrest at the G0/G1 phase and correspondingly decrease the percentage of S phase cells in both U87 and U251 cell lines. Moreover, it was found that silenced zinc finger antisense 1 could impair migration and invasion by inhibiting the epithelial–mesenchymal transition through reducing the expression of MMP2, MMP9, N-cadherin, Integrin β1, ZEB1, Twist, and Snail as well as increasing E-cadherin level in glioma. Taken together, our data identified that zinc finger antisense 1 might act as a valuable prognostic biomarker and potential therapeutic target for glioma.

Publisher

IOS Press

Subject

General Medicine

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