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Related Experiment Video

Updated: Feb 28, 2026

Network Pharmacology Prediction and Experimental Validation of Trichosanthes-Fritillaria thunbergii Action Mechanism Against Lung Adenocarcinoma

Network Pharmacology Prediction and Experimental Validation of Trichosanthes-Fritillaria thunbergii Action Mechanism Against Lung Adenocarcinoma

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The KEAP1-NRF2 System in Cancer.

Keiko Taguchi¹, Masayuki Yamamoto¹

¹Department of Medical Biochemistry, Graduate School of Medicine, Tohoku University, Sendai, Japan.

Frontiers in Oncology

|May 20, 2017

Summary

Nuclear factor erythroid 2-related factor 2 (NRF2) plays a key role in cancer progression and drug resistance. Targeting NRF2 through inhibition or induction offers potential therapeutic strategies for various cancers.

Area of Science:

Oncology
Molecular Biology
Cancer Genomics

Background:

Cancer cells adapt to their microenvironment and propagate, often driven by mutations in tumor suppressor genes or oncogenes.
Genomic analyses reveal frequent alterations in KEAP1/NRF2 pathway genes (KEAP1, NRF2) and other key cancer genes (TP53, CDKN2A, PTEN, PIK3CA).
Aberrant NRF2 activation, caused by KEAP1/NRF2 mutations or disrupted KEAP1-NRF2 binding, promotes cancer cell resistance to drugs and reactive oxygen species (ROS), and drives metabolic reprogramming.

Purpose of the Study:

To explore the role of Nuclear factor erythroid 2-related factor 2 (NRF2) as a therapeutic target in cancer.
To review the dual strategies of NRF2 inhibition and induction for cancer treatment.
To discuss the potential of diagnosing NRF2 activation for personalized cancer therapy.

Keywords:

KEAP1 NRF2 cancer cancer therapy metabolic reprogramming

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Main Methods:

Comprehensive genomic analyses to identify somatic mutations and alterations in cancer-related genes, particularly focusing on the KEAP1-NRF2 pathway.
Review of existing and developing therapeutic strategies targeting NRF2, including inhibitors and inducers.
Analysis of the impact of NRF2 dysregulation on cancer cell phenotypes, such as drug resistance and metabolic reprogramming.

Main Results:

NRF2 pathway alterations are common in various cancers and contribute to malignant phenotypes.
Aberrant NRF2 activation confers significant resistance to anticancer drugs and ROS.
NRF2 dysregulation drives metabolic reprogramming in cancer cells, enhancing survival and proliferation.

Conclusions:

NRF2 is a critical therapeutic target in oncology due to its role in promoting cancer cell survival and resistance.
NRF2 inhibitors show promise for 'NRF2-addicted' cancers, necessitating diagnostic methods for patient selection.
NRF2 inducers, currently developed for non-cancerous conditions, may also serve as adjuncts in cancer chemotherapy or in combination with NRF2 inhibitors.