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The deubiquitinating enzyme USP5 promotes pancreatic cancer via modulating cell cycle regulators

Brajesh P Kaistha1, Anja Krattenmacher1, Johannes Fredebohm2

  • 1Department of Medicine, Division of Gastroenterology, Endocrinology and Metabolism, Philipps-University Marburg, Marburg, Germany.

Oncotarget
|October 15, 2017
PubMed

Insights

Pancreatic ductal adenocarcinoma (PDAC) is a lethal cancer. Researchers identified USP5 as crucial for PDAC cell survival and proliferation, suggesting it as a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Pancreatic ductal adenocarcinoma (PDAC) has a very low survival rate, necessitating new therapeutic targets.
  • Deubiquitinases are emerging as promising drug targets in cancer therapy.

Purpose of the Study:

  • To identify novel genes involved in pancreatic cancer survival and progression using a functional genomics screen.
  • To investigate the role of the deubiquitinase USP5 in PDAC.

Main Methods:

  • A short-hairpin RNA (shRNA) library screen was performed in pancreatic cancer cells.
  • Gene expression analysis in human pancreatic cancer tissues.
  • Knockdown experiments in cell culture (2D and 3D) and in vivo models.
  • Cell cycle analysis, DNA damage assessment, and apoptosis assays.

Main Results:

  • USP5 was identified as a candidate gene in the shRNA screen and found to be upregulated in human PDAC tissues.
  • Knockdown of USP5 inhibited pancreatic cancer cell proliferation and survival.
  • USP5 knockdown led to G1/S phase cell cycle arrest, DNA damage accumulation, p27 upregulation, and increased apoptosis.

Conclusions:

  • USP5 is essential for pancreatic cancer cell proliferation and survival.
  • USP5 represents a potential novel therapeutic target for pancreatic ductal adenocarcinoma.

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