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Correction: Sekar et al. Concussion/Mild Traumatic Brain Injury (TBI) Induces Brain Insulin Resistance: A Positron Emission Tomography (PET) Scanning Study. <i>Int. J. Mol. Sci.</i> 2021, <i>22</i>, 9005.

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Sterol regulatory element-binding protein 1 inhibitors decrease pancreatic cancer cell viability and proliferation.

Siqingaowa1, Sathiya Sekar1, Venkat Gopalakrishnan1

  • 1Department of Pharmacology, College of Medicine, University of Saskatchewan, 107 Wiggin's Road, Saskatoon, SK S7N 5E5, Canada.

Biochemical and Biophysical Research Communications
|May 10, 2017
PubMed
Summary

Sterol regulatory element-binding protein1 (SREBP1) inhibitors, fatostatin and PF429242, significantly reduced pancreatic cancer cell growth. These SREBP1 inhibitors decreased key lipid synthesis proteins and mutant p53, suggesting a therapeutic target for pancreatic cancer.

Keywords:
FatostatinLipid metabolismMIA PaCa-2 cellsPF429242Pancreatic cancerSREBP1

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Sterol regulatory element-binding protein1 (SREBP1) is crucial for lipid homeostasis and implicated in various cancers.
  • SREBP1 overactivation and lipid biogenesis are hallmarks of prostate cancer, endometrial cancer, and glioblastoma.
  • The role of SREBP1 in pancreatic cancer progression remains largely unexplored.

Purpose of the Study:

  • To investigate the effect of SREBP1 activation suppression on pancreatic cancer cell proliferation.
  • To analyze the impact of SREBP1 inhibitors (fatostatin, PF429242) on downstream signaling pathways.
  • To evaluate the potential of SREBP1 as a therapeutic target in pancreatic cancer.

Main Methods:

  • In vitro study using MIA PaCa-2 pancreatic cancer cells.
  • Treatment with SREBP1 inhibitors fatostatin and PF429242.
  • Cell growth inhibition assays, Western blot analysis to assess protein levels.

Main Results:

  • Fatostatin and PF429242 inhibited MIA PaCa-2 cell growth in a time- and concentration-dependent manner.
  • Inhibitors significantly decreased active SREBP1 levels and its downstream targets: fatty acid synthase (FAS), stearoyl-CoA desaturase-1 (SCD-1), and hydroxymethylglutaryl-CoA reductase (HMGCoAR).
  • Levels of mutant tumor suppressor protein p53 were also reduced by the inhibitors.

Conclusions:

  • SREBP1 activation contributes to pancreatic cancer cell growth.
  • SREBP1 inhibitors demonstrate potential as therapeutic agents for pancreatic cancer management.
  • Targeting SREBP1 offers a promising strategy for controlling pancreatic cancer proliferation.