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Updated: Nov 15, 2025

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo
Published on: July 20, 2019
[Effect of Nrf2 in tumor progression and its inhibitors in cancer therapy]
1School of Basic Medical Sciences, Xinxiang Medical University Xinxiang 453003, China.
Abstract:
Nrf2 is the key transcription factor mainly for regulating oxidative homeostasis and cytoprotective responses against oxidative stress. Nrf2/Keap1 pathway is one of the most important cellular defense mechanisms against endogenous or exogenous oxidative stress. With its activation, a wide range of stress-related genes is transactivated to restore the cellular homeostasis. Recent studies revealed that the aberrant activation of Nrf2 is related to the malignant progression, chemotherapeutic drug resistance and poor prognosis. Nrf2 plays a crucial role in cancer malignancy and chemotherapeutic resistance by controlling the intracellular redox homeostasis through the activation of cytoprotective antioxidant genes. Nrf2 inhibitor containing many natural products has been deemed as a novel therapeutic strategy for human malignancies. This article reviews the progress of studies of the Nrf2/Keap1 pathway, and its biological impact in solid malignancies and molecular mechanisms for causing Nrf2 hyperactivation in cancer cells. In conclusion, we summarized the deve-lopment of Nrf2 inhibitors in recent years, in the expectation of providing reference for further drug development and clinical studies.
Insights
The Nrf2/Keap1 pathway regulates cellular defense against oxidative stress. Aberrant Nrf2 activation drives cancer progression and drug resistance, making Nrf2 inhibitors a promising therapeutic strategy for malignancies.
Area of Science:
- Molecular Biology
- Cellular Biology
- Oncology
Background:
- Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor crucial for maintaining oxidative homeostasis and cellular defense against oxidative stress.
- The Nrf2/Keap1 pathway is a primary cellular mechanism protecting against endogenous and exogenous oxidative damage, activating numerous stress-response genes to restore cellular balance.
- Recent research indicates that dysregulated Nrf2 activation is linked to cancer progression, resistance to chemotherapy, and poorer patient outcomes.
Purpose of the Study:
- To review the current understanding of the Nrf2/Keap1 pathway's role in solid malignancies.
- To explore the molecular mechanisms underlying Nrf2 hyperactivation in cancer cells.
- To summarize the development of Nrf2 inhibitors as a potential therapeutic approach for cancer.
Main Methods:
- Literature review of studies on the Nrf2/Keap1 pathway.
- Analysis of Nrf2's biological impact in solid tumors.
- Investigation of molecular mechanisms driving Nrf2 hyperactivation.
Main Results:
- Nrf2 plays a significant role in cancer malignancy and chemoresistance by modulating intracellular redox balance via cytoprotective antioxidant genes.
- Aberrant Nrf2 activation is associated with malignant progression and poor prognosis in cancer patients.
- Natural products containing Nrf2 inhibitors are being explored as novel therapeutic agents.
Conclusions:
- The Nrf2/Keap1 pathway is a critical factor in cancer development and treatment resistance.
- Understanding Nrf2 hyperactivation mechanisms is key to developing effective cancer therapies.
- Continued development of Nrf2 inhibitors holds promise for future cancer drug discovery and clinical application.
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