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Updated: Mar 31, 2026

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer
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Role of CSL-dependent and independent Notch signaling pathways in cell apoptosis

Chong Zeng1,2, Rui Xing3, Jing Liu4

  • 1Department of Immunobiology, Institute of Tissue Transplantation and Immunology, Jinan University, Guangzhou, 510632, China.

Apoptosis : an International Journal on Programmed Cell Death
|October 27, 2015
PubMed

Insights

This review explores how Notch signaling, a conserved biological pathway, influences cell apoptosis. It details CSL-dependent and independent pathways, offering new insights into cell death mechanisms.

Area of Science:

  • Cellular Biology
  • Molecular Mechanisms
  • Developmental Biology

Background:

  • Apoptosis is a fundamental biological process involving intricate molecular signaling pathways.
  • Notch signaling is an evolutionarily conserved pathway crucial for development, tissue homeostasis, and immune regulation.

Purpose of the Study:

  • To review recent advances in understanding the roles of CSL-dependent and independent Notch signaling in cell apoptosis.
  • To elucidate the molecular mechanisms underlying Notch-mediated apoptosis.

Main Methods:

  • Literature review focusing on novel research in Notch signaling and apoptosis.
  • Analysis of molecular mechanisms involving CSL-dependent and CSL-independent pathways.
  • Examination of key signaling molecules such as CSL, NIC, Hes-1, PTEN, AKT, mTOR, and mTORC2.

Main Results:

  • CSL-dependent Notch signaling regulates apoptosis via the Hes-1-PTEN-AKT-mTOR pathway.
  • CSL-independent Notch signaling potentially mediates apoptosis through the NIC-mTORC2-AKT-mTOR pathway.
  • These distinct pathways offer new perspectives on the regulation of programmed cell death.

Conclusions:

  • Notch signaling plays a significant role in regulating cell apoptosis through both CSL-dependent and independent mechanisms.
  • Understanding these pathways provides novel insights into apoptotic mechanisms and potential therapeutic targets.
Keywords:
ApoptosisCSL-dependent NotchCSL-independent NotchCellmTORC

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