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Upregulation of long noncoding RNA LINC00152 promotes proliferation and metastasis of esophageal squamous cell carcinoma

Authors Yang Y, Sun X, Chi C, Liu Y, Lin C, Xie D, Shen X, Lin X

Received 19 December 2018

Accepted for publication 20 April 2019

Published 21 May 2019 Volume 2019:11 Pages 4643—4654


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Professor Nakshatri

Yi Yang,1,* Xiangwei Sun,2,* Chuang Chi,3 Yu Liu,3 Chaoxi Lin,3 Deyao Xie,3 Xian Shen,2 Xiaoming Lin3

1Department of Clinical Skills Experiments Center, Wenzhou Medical University, Wenzhou, Zhejiang 325035, People’s Republic of China; 2Department of General Surgery, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325003, People’s Republic of China; 3Department of Thoracic Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325003, People’s Republic of China

*These authors contributed equally to this work

Esophageal cancer is a major cause of cancer-related mortality worldwide. The long noncoding RNA LINC00152 has been confirmed to play an oncogenic role in many cancers. However, the expression pattern and function of LINC00152 in human esophageal squamous cell carcinoma (ESCC) remain unclear.
Materials and methods: We evaluated LINC00152 expression in ESCC by qPCR and in situ hybridization. Proliferation, apoptosis, cell cycle, migration and invasion were examined in ESCC cells knocked down for LINC00152 knockdown by siRNA. Furthermore, an mRNA microarray was performed in ESCC cells with LINC00152 knockdown.
Results: LINC00152 was significantly upregulated in human ESCC clinical samples (P<0.001) and cell lines (P=0.008), and LINC00152 overexpression was related to lymphatic metastasis (P=0.03) and advanced pTNM classification (P=0.005). Furthermore, ESCC patients with LINC00152 overexpression had significantly shorter overall survival (P=0.007), and LINC00152 overexpression was an independent risk factor for overall survival of ESCC patients. LINC00152 knockdown inhibited the proliferation, migration and invasion of ESCC cells in vitro. In addition, mechanistic investigations through mRNA array and immunoblot analyses demonstrated that LINC00152 regulated the expression of several cell cycle-related proteins and SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptors) interactions in vesicular transport pathway proteins.
Conclusion: Our research indicated that LINC00152 exhibits oncogenic functions in ESCC and may represent a potential new target for ESCC therapy.

Keywords: LINC00152, esophageal squamous cell carcinoma, proliferation, metastasis

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