Long non‑coding RNA PCED1B‑AS1 promotes pancreatic ductal adenocarcinoma progression by regulating the miR‑411‑3p/HIF‑1α axis
- Yi Zhang
- Huan Ma
- Chang Chen
Affiliations: Department of Gastroenterology, The People's Hospital of China Three Gorges University and The First People's Hospital of Yichang, Yichang, Hubei 443000, P.R. China, Department of Gastroenterology, Qingdao Municipal Hospital, Qingdao, Shandong 266000, P.R. China
- Published online on: May 20, 2021 https://doi.org/10.3892/or.2021.8085
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An increasing number of studies have shown that long non‑coding RNAs (lncRNAs) are crucially involved in tumorigenesis. However, the biological functions, underlying mechanisms and clinical value of lncRNA PC‑esterase domain containing 1B‑antisense RNA 1 (PCED1B‑AS1) in pancreatic ductal adenocarcinoma (PDAC) have not been determined, to the best of our knowledge. In the present study, the expression of PCED1B‑AS1, microRNA (miR)‑411‑3p and hypoxia inducible factor (HIF)‑1α mRNA in 47 cases of PDAC tissues were detected using reverse transcription‑quantitative (RT‑q)PCR. Moreover, the effects of PCED1B‑AS1 on the biological behaviors of PDAC cells were assessed using Cell Counting Kit‑8, EdU staining and Transwell assays. Bioinformatics analysis, RT‑qPCR, western blotting, dual luciferase reporter gene and RNA immunoprecipitation assays were performed to determine the regulatory relationships between PCED1B‑AS1, miR‑411‑3p and HIF‑1α. We demonstrated that PCED1B‑AS1 was significantly upregulated in PDAC tumor tissues, and its expression was associated with advanced Tumor‑Node‑Metastasis stage and lymph node metastasis. PCED1B‑AS1 knockdown inhibited PDAC cell proliferation, invasion as well as epithelial‑mesenchymal transition (EMT) in vitro. Mechanistically, PCED1B‑AS1 was shown to target miR‑411‑3p, resulting in the upregulation of HIF‑1α. In conclusion, PCED1B‑AS1 expression was upregulated in PDAC tissues and cells, and it participated in promoting the proliferation, invasion and EMT of cancer cells by modulating the miR‑411‑3p/HIF‑1α axis.