Startseite PCAT1 induced by transcription factor YY1 promotes cholangiocarcinoma proliferation, migration and invasion by sponging miR-216a-3p to up-regulate oncogene BCL3
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PCAT1 induced by transcription factor YY1 promotes cholangiocarcinoma proliferation, migration and invasion by sponging miR-216a-3p to up-regulate oncogene BCL3

  • Dongsheng Sun ORCID logo , Yuqiao Zhao , Weina Wang , Canghai Guan , Zengtao Hu , Lang Liu und Xingming Jiang EMAIL logo
Veröffentlicht/Copyright: 23. Oktober 2020

Abstract

This study was designed to illustrate the function and role of PCAT1 in CCA. The relative expression was confirmed by RT-qPCR and western blot. The biological function of PCAT1 was evaluated by CCK8, EdU, colony formation, wound healing, transwell, and subcutaneous tumor formation assays. Protein levels of EMT markers were measured by western blot. The binding relationship was predicted by JASPAR and starBase. The binding of YY1 to PCAT1 promoter was assessed by ChIP and luciferase reporter. The binding capacity between miR-216a-3p and PCAT1 as well as BCL3 was assessed by luciferase reporter and AGO2-RIP assays. In this study, we found that PCAT1 was up-regulated in CCA tissues and cells, and the PCAT1 overexpression was associated with poor prognosis. Moreover, PCAT1 was assessed as an independent risk factor of prognosis for CCA patients. Amplified PCAT1 was found to promote tumor proliferation, migration, invasion and EMT process, whereas PCAT1 knockdown inhibited these malignant phenotypes. Mechanistically, PCAT1 was predominantly localized in the cytoplasm and competitively bound miR-216a-3p to increase BCL3 expression. In addition, PCAT1 was activated by transcription factor YY1. This study revealed that PCAT1 acted as an oncogene in CCA, and the YY1/PCAT1/miR-216a-3p/BCL3 axis exhibited critical functions in CCA progression.


Corresponding author: Xingming Jiang, Department of General Surgery, The 2nd Affiliated Hospital of Harbin Medical University, No. 148 BaoJian-ro, Harbin150086, Heilongjiang, China, E-mail:
Dongsheng Sun, Yuqiao Zhao and Weina Wang: These authors contributed equally to this work.
  1. Author contribution: All the authors have accepted responsibility for the entire content of this submitted manuscript and approved submission.

  2. Research funding: None declared.

  3. Conflict of interest statement: The authors declare that they have no competing interests.

  4. Data availability statement: The data used to support the findings of this study are available from the corresponding author upon request.

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Received: 2020-08-09
Accepted: 2020-10-12
Published Online: 2020-10-23
Published in Print: 2021-01-27

© 2020 Walter de Gruyter GmbH, Berlin/Boston

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