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Int J Oncol. 2018 Sep 27. doi: 10.3892/ijo.2018.4574. [Epub ahead of print]

Long non-coding RNA CUDR promotes malignant phenotypes in pancreatic ductal adenocarcinoma via activating AKT and ERK signaling pathways.

Author information

1
Department of Pancreatic-Biliary Surgery, Changzheng Hospital, Second Military Medical University, Shanghai 200003, P.R. China.
2
Key Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of The Chinese Academy of Sciences, Shanghai 200031, P.R. China.
3
The First Department of Biliary Surgery, Eastern Hepatobiliary Surgery Hospital, Shanghai 200433, P.R. China.
4
Department of Pancreatic Surgery, Changhai Hospital, Second Military Medical University, Shanghai 200433, P.R. China.
5
General Surgical Department, Sir Run Run Shaw Hospital affiliated with The Zhejiang University School of Medicine, Hangzhou, Zhejiang 310016, P.R. China.

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies, with a marked potential for invasion and metastasis. Emerging evidence has suggested that dysregulation of long non-coding RNAs (lncRNAs) is associated with the development of multiple types of cancer. However, the function of lncRNAs in PDAC is poorly known. In the present study, a microarray assay was used to screen for differently expressed lncRNAs in PDAC and it was identified that cancer upregulated drug resistance (CUDR) was upregulated in PDAC. CUDR increased PDAC cell proliferation, migration and invasion, inhibited apoptosis, and promoted drug resistance; it also regulated the PDAC cell epithelial-mesenchymal transition. The CUDR-induced PDAC malignant phenotypes is via the protein kinase B and extracellular-signal-regulated kinase signaling pathways. Downregulation of CUDR may be a novel therapeutic strategy to prevent PDAC development and drug resistance in the future.

PMID:
30272271
DOI:
10.3892/ijo.2018.4574

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