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

作者：Xing Liang, Meiyan Qi, Rui Wu, An‐An Liu, Danlei Chen, Liang Tang, Jun Chen, Xiangui Hu, Wěi Li, Lixing Zhan, Chenghao Shao · 发表于：International Journal of Oncology · 年份：2018 · DOI：10.3892/ijo.2018.4574 · 被引用次数：17 · 研究领域：Cancer-related molecular mechanisms research、RNA modifications and cancer、MicroRNA in disease regulation

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.