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Int J Biol Macromol. 2017 Sep;102:718-728. doi: 10.1016/j.ijbiomac.2017.03.123. Epub 2017 Mar 23.

The over expression of long non-coding RNA ANRIL promotes epithelial-mesenchymal transition by activating the ATM-E2F1 signaling pathway in pancreatic cancer: An in vivo and in vitro study.

Author information

1
Department of Hepatobiliary Surgery, Fujian Provincial Hospital, Fujian Medical University, Fuzhou 350001, P.R. China; Department of General Surgery, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, PR China; Research Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
2
Department of General Surgery, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, PR China; Research Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
3
Department of General Surgery, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, PR China; Research Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China; Department of Hepatobiliary Surgery, Union Hospital, Fujian Medical University, Fuzhou 350001, PR China.
4
Department of Hepatobiliary Surgery, Union Hospital, Fujian Medical University, Fuzhou 350001, PR China.
5
Department of Hepatobiliary Surgery, Fujian Provincial Hospital, Fujian Medical University, Fuzhou 350001, P.R. China.
6
Department of Hepatobiliary Surgery, Fujian Provincial Hospital, Fujian Medical University, Fuzhou 350001, P.R. China. Electronic address: yifeng0887@126.com.
7
Department of Hepatobiliary Surgery, Fujian Provincial Hospital, Fujian Medical University, Fuzhou 350001, P.R. China. Electronic address: wangyd358@163.com.

Abstract

This study aims to investigate the roles of lncRNA ANRIL in epithelial-mesenchymal transition (EMT) by regulating the ATM-E2F1 signaling pathway in pancreatic cancer (PC). PC rat models were established and ANRIL overexpression and interference plasmids were transfected. The expression of ANRIL, EMT markers (E-cadherin, N-cadherin and Vimentin) and ATM-E2F1 signaling pathway-related proteins (ATM, E2F1, INK4A, INK4B and ARF) were detected. Small molecule drugs were applied to activate and inhibit the ATM-E2F1 signaling pathway. Transwell assay and the scratch test were adopted to detect cell invasion and migration abilities. ANRIL expression in the PC cells was higher than in normal pancreatic duct epithelial cells. In the PC rat models and PC cells, ANRIL interference promoted the expressions of INK4B, INK4A, ARF and E-cadherin, while reduced N-cadherin and Vimentin expression. Over-expressed ANRIL decreased the expression of INK4B, INK4A, ARF and E-cadherin, but raised N-cadherin and Vimentin expressions. By inhibiting the ATM-E2F1 signaling pathway in PC cells, E-cadherin expression increased but N-cadherin and Vimentin expressions decreased. After ANRIL was silenced or the ATM-E2F1 signaling pathway inhibited, PC cell migration and invasion abilities were decreased. In conclusion, over-expression of lncRNA ANRIL can promote EMT of PC cells by activating the ATM-E2F1 signaling pathway.

KEYWORDS:

Epithelial-mesenchymal transition and rat model; Long non-coding RNA ANRIL; Pancreatic cancer; the ATM-E2F1 signaling pathway

PMID:
28344092
DOI:
10.1016/j.ijbiomac.2017.03.123
[Indexed for MEDLINE]

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