Decoding the NRF2-NOTCH Crosstalk in Lung Cancer-An Update

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.