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NICD inhibits cell proliferation and promotes apoptosis and autophagy in PC12 cells

Bo Li1, Ping Duan1, Xuefei Han2

  • 1Department of Physiology, Zhengzhou University, Zhengzhou, Henan 450001, P.R. China.

Molecular Medicine Reports
|July 6, 2017
PubMed

Insights

Overexpressing the Notch1 intracellular domain (NICD) in pheochromocytoma cells promotes apoptosis and inhibits proliferation. This suggests NICD may be a potential therapeutic target for pheochromocytoma treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Pheochromocytoma, an adrenal medulla tumor, is currently only treated by surgical resection.
  • The Notch1 signaling pathway is a potential therapeutic target, but the role of its intracellular domain (NICD) in pheochromocytoma is unclear.

Purpose of the Study:

  • To investigate the effect of Notch1 intracellular domain (NICD) overexpression on pheochromocytoma cell growth and identify underlying mechanisms.

Main Methods:

  • Utilized a tetracycline-inducible system for NICD overexpression in the PC12 pheochromocytoma cell line.
  • Assessed cell cycle distribution and apoptosis using flow cytometry.
  • Examined autophagy-related protein expression (LC3B, Beclin 1, ATG5, ATG7) via Western blot analysis.

Main Results:

  • NICD overexpression significantly promoted apoptosis and suppressed proliferation by inducing S-phase arrest.
  • NICD stimulation led to increased expression of autophagy markers: LC3B, Beclin 1, ATG5, and ATG7.

Conclusions:

  • NICD overexpression in pheochromocytoma cells induces apoptosis, inhibits proliferation, and stimulates autophagy.
  • These findings highlight the potential of NICD as a therapeutic strategy for pheochromocytoma.

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