Department of Pancreatic-Biliary Surgery, Changzheng Hospital, Second Military Medical University, Shanghai 200003, P.R. China.
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.
Int J Oncol. 2018 Dec;53(6):2671-2682. doi: 10.3892/ijo.2018.4574. Epub 2018 Sep 27.
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.
胰腺导管腺癌 (PDAC) 是最致命的恶性肿瘤之一，具有明显的侵袭和转移潜力。新出现的证据表明，长非编码 RNA (lncRNA) 的失调与多种类型癌症的发展有关。然而，lncRNA 在 PDAC 中的功能知之甚少。在本研究中，使用微阵列分析筛选 PDAC 中差异表达的 lncRNA，发现癌症上调耐药性 (CUDR) 在 PDAC 中上调。CUDR 增加 PDAC 细胞增殖、迁移和侵袭，抑制细胞凋亡，促进耐药性；它还调节 PDAC 细胞上皮-间充质转化。CUDR 诱导的 PDAC 恶性表型是通过蛋白激酶 B 和细胞外信号调节激酶信号通路。下调 CUDR 可能是未来预防 PDAC 发展和耐药性的一种新的治疗策略。
