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Related Concept Videos

Notch Signaling Pathway03:14

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The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not...
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The probability of having two carbon-13 atoms next to each other is negligible because of the low natural abundance of carbon-13. Consequently, peak splitting due to carbon-carbon spin-spin coupling is not observed in spectra. However, protons up to three sigma bonds away split the carbon signal according to the n+1 rule, resulting in complicated spectra.
A broadband decoupling technique is used to simplify these complex, sometimes overlapping, signals. Broadband decoupling relies on a...
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Decoding the NRF2-NOTCH Crosstalk in Lung Cancer-An Update.

Angelo Sparaneo1, Filippo Torrisi2, Floriana D'Angeli3

  • 1Laboratory of Oncology, Fondazione IRCCS Casa Sollievo della Sofferenza, 71013 San Giovanni Rotondo, Italy.

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|June 26, 2025
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Summary

The Nuclear factor erythroid 2-related factor 2 (NRF2) and NOTCH signaling pathways crosstalk impacts lung cancer progression and therapy resistance. Understanding this interplay is key to developing new lung cancer treatments.

Keywords:
NOTCHNRF2lung canceroxidative stressresistance

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • The Nuclear factor erythroid 2-related factor 2 (NRF2) and NOTCH signaling pathways are critical in solid cancers, particularly lung cancer.
  • Dysregulation of NRF2 and NOTCH independently or convergently contributes to tumor growth, therapy resistance, and oxidative stress.
  • The NRF2/NOTCH interplay influences metabolic reprogramming and the tumor microenvironment (TME).

Purpose of the Study:

  • To explore the molecular mechanisms of NRF2-NOTCH crosstalk in lung cancer.
  • To highlight the impact of genetic and epigenetic deregulation on neoplastic processes, TME, and metabolic reprogramming.
  • To discuss therapeutic strategies targeting the NRF2-NOTCH network for improved lung cancer treatment.

Main Methods:

  • Review of current scientific literature on NRF2-NOTCH signaling in lung cancer.
  • Analysis of molecular mechanisms, genetic/epigenetic alterations, and their impact on cancer progression.
  • Exploration of the role in metabolic reprogramming and TME modulation.

Main Results:

  • NRF2-NOTCH crosstalk significantly impacts lung cancer progression, tumor growth, and therapeutic resistance.
  • This interplay drives metabolic reprogramming and reshapes the tumor microenvironment, promoting malignancy.
  • The precise role of NRF2-NOTCH interaction in supporting or suppressing lung tumor phenotypes requires further elucidation.

Conclusions:

  • Targeting the NRF2-NOTCH regulatory network presents promising therapeutic opportunities for lung cancer.
  • Understanding this crosstalk can help overcome drug resistance and improve patient outcomes.
  • Further research into the NRF2-NOTCH axis is crucial for advancing lung cancer therapy.