Oncotarget

Research Papers:

Long noncoding RNA MALAT1 promotes malignant development of esophageal squamous cell carcinoma by targeting β-catenin via Ezh2

Wei Wang _, Yunan Zhu, Sanni Li, Xinfeng Chen, Guozhong Jiang, Zhibo Shen, Yamin Qiao, Liping Wang, Pengyuan Zheng and Yi Zhang

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Oncotarget. 2016; 7:25668-25682. https://doi.org/10.18632/oncotarget.8257

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Abstract

Wei Wang1,2, Yunan Zhu2, Sanni Li2, Xinfeng Chen1,3, Guozhong Jiang4, Zhibo Shen1,3, Yamin Qiao1,3, Liping Wang1, Pengyuan Zheng6, Yi Zhang1,3,5,7

1Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China

2The Third People’s Hospital of Zhengzhou, Zhengzhou, Henan 450000, China

3Biotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China

4Department of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China

5Engineering Key Laboratory for Cell Therapy of Henan Province, Zhengzhou, Henan 450052, China

6Department of Gastroenterology, The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 470000, China

7School of Life Sciences, Zhengzhou University, Zhengzhou, Henan 450001, China

Correspondence to:

Yi Zhang, email: [email protected]

Keywords: ESCC, lncrna, MALAT1, β-catenin, Ezh2

Received: August 26, 2015    Accepted: March 07, 2016    Published: March 22, 2016

ABSTRACT

Evidences have shown that lncRNAs involve in the initiation and progression of various cancers including esophageal squamous cell carcinoma (ESCC). The aberrant expression of lncRNA MALAT1 was investigated in 106 paired ESCC tissues and adjacent non-cancerous tissues by qRT-PCR. Down-regulated MALAT1 and Ezh2 over-expression plasmid were constructed respectively to analyze the expression of β-catenin, Lin28 and Ezh2 genes. We found that the MALAT1 expression level was higher in human ESCC tissues (P=0.0011), which was closely correlated with WHO grade (P=0.0395, P=0.0331), lymph node metastasis (P=0.0213) and prognosis (P=0.0294). Silencing of MALAT1 expression inhibited cell proliferation, migration and tumor sphere formation, while increasing cell apoptosis of esophageal cancer in vitro. Down-regulation of MALAT1 decreased the expression of β-catenin, Lin28 and Ezh2 genes, while over-expressed Ezh2 combined with MALAT1 down-regulation completely reversed the si-MALAT1-mediated repression of β-catenin and Lin28 in esophageal cancer cells. Animal experiments showed that knockdown of MALAT1 decreased tumor formation and improved survival. MALAT1 promotes the initiation and progression of ESCC, suggesting that inhibition of MALAT1 might be a potential target for treatment of ESCC.


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