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Long non‑coding RNA PCED1B‑AS1 promotes pancreatic ductal adenocarcinoma progression by regulating the miR‑411‑3p/HIF‑1α axis

  • Authors:
    • Yi Zhang
    • Huan Ma
    • Chang Chen
  • View Affiliations / Copyright

    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
    Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY 4.0].
  • Article Number: 134
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    Published online on: May 20, 2021
       https://doi.org/10.3892/or.2021.8085
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Abstract

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.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang Y, Ma H and Chen C: Long non‑coding RNA PCED1B‑AS1 promotes pancreatic ductal adenocarcinoma progression by regulating the miR‑411‑3p/HIF‑1α axis. Oncol Rep 46: 134, 2021.
APA
Zhang, Y., Ma, H., & Chen, C. (2021). Long non‑coding RNA PCED1B‑AS1 promotes pancreatic ductal adenocarcinoma progression by regulating the miR‑411‑3p/HIF‑1α axis. Oncology Reports, 46, 134. https://doi.org/10.3892/or.2021.8085
MLA
Zhang, Y., Ma, H., Chen, C."Long non‑coding RNA PCED1B‑AS1 promotes pancreatic ductal adenocarcinoma progression by regulating the miR‑411‑3p/HIF‑1α axis". Oncology Reports 46.1 (2021): 134.
Chicago
Zhang, Y., Ma, H., Chen, C."Long non‑coding RNA PCED1B‑AS1 promotes pancreatic ductal adenocarcinoma progression by regulating the miR‑411‑3p/HIF‑1α axis". Oncology Reports 46, no. 1 (2021): 134. https://doi.org/10.3892/or.2021.8085
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang Y, Ma H and Chen C: Long non‑coding RNA PCED1B‑AS1 promotes pancreatic ductal adenocarcinoma progression by regulating the miR‑411‑3p/HIF‑1α axis. Oncol Rep 46: 134, 2021.
APA
Zhang, Y., Ma, H., & Chen, C. (2021). Long non‑coding RNA PCED1B‑AS1 promotes pancreatic ductal adenocarcinoma progression by regulating the miR‑411‑3p/HIF‑1α axis. Oncology Reports, 46, 134. https://doi.org/10.3892/or.2021.8085
MLA
Zhang, Y., Ma, H., Chen, C."Long non‑coding RNA PCED1B‑AS1 promotes pancreatic ductal adenocarcinoma progression by regulating the miR‑411‑3p/HIF‑1α axis". Oncology Reports 46.1 (2021): 134.
Chicago
Zhang, Y., Ma, H., Chen, C."Long non‑coding RNA PCED1B‑AS1 promotes pancreatic ductal adenocarcinoma progression by regulating the miR‑411‑3p/HIF‑1α axis". Oncology Reports 46, no. 1 (2021): 134. https://doi.org/10.3892/or.2021.8085
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