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Yin Yang-1 suppresses pancreatic ductal adenocarcinoma cell proliferation and tumor growth by regulating SOX2OT-SOX2 axis. | LitMetric

Yin Yang-1 suppresses pancreatic ductal adenocarcinoma cell proliferation and tumor growth by regulating SOX2OT-SOX2 axis.

Cancer Lett

Pancreas Center, Department of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, PR China; Pancreas Institute of Nanjing Medical University, Nanjing 210029, PR China. Electronic address:

Published: November 2017

AI Article Synopsis

  • The transcription regulator YY1 functions as a tumor suppressor in pancreatic ductal adenocarcinoma (PDAC) by inhibiting cell proliferation.
  • Overexpressing YY1 leads to reduced levels of long non-coding RNA SOX2OT and its target gene SOX2, which are linked to PDAC progression.
  • The study indicates that YY1's anti-proliferative effects are connected to a decrease in SOX2 expression via the suppression of SOX2OT, suggesting potential diagnostic and therapeutic opportunities for targeting these molecules in PDAC.

Article Abstract

The transcription regulator Yin Yang-1 (YY1) serves as a tumor suppressor in pancreatic ductal adenocarcinoma (PDAC). However, the function of YY1 in proliferation of PDAC cells remains to be clarified. In this study, we found that overexpression of YY1 suppressed proliferation and decreased the expression of long non-coding RNA (lncRNA) SOX2OT and its potential target gene SOX2 in PDAC cells. Luciferase reporter, electrophoretic mobility shift (EMSA), and chromatin immunoprecipitation (ChIP) assays revealed binding of YY1 to the SOX2OT promoter. Moreover, YY1 suppressed PDAC cell proliferation through SOX2OT transcriptional inhibition and subsequent decreased SOX2 expression. In addition, YY1 expression was statistically negatively correlated with SOX2OT and SOX2 expression in PDAC tissues and lower level expression of SOX2OT predicted better outcome in PDAC patients. These results confirmed the anti-proliferation effect of YY1 on PDAC cells, which was associated with SOX2 down-regulation in a SOX2OT-dependent mechanism. Although other undiscovered mechanisms may be involved in the YY1-mediated tumor suppression role, the present study suggests that SOX2OT may act as a tumor promotor in PDAC and may represent a valuable diagnostic and therapeutic target.

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Source
http://dx.doi.org/10.1016/j.canlet.2017.08.032DOI Listing

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