Nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2) in non-small cell lung cancer
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Updated: Dec 30, 2025

A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia
Published on: December 4, 2018
Zhi Zeng1, Zi-Yao Wang2, Yu-Kun Li3
1Department of Pathology, Xianning Central Hospital, The First Affiliated Hospital of Hubei University of Science and Technology, Xianning 437000, PR China.
Abstract:
Nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2) is a transcription factor that can regulate downstream target gene expression. Kelch-like ECH-associated protein 1 (Keap1) negatively regulates Nrf2 activation and translocation to target its 26S proteasomal degradation. It has been widely reported that the Keap1/Nrf2 pathway is associated with tumorigenesis, chemotherapy resistance and progression and development of non-small cell lung cancer (NSCLC). High expression of Nrf2 and low abundance of Keap1 contribute to the abnormalities and unrealistic treatment prognosis of NSCLC. Therefore, elucidating the role and potential mechanism of Nrf2 in NSCLC is essential for understanding tumorigenesis and for the development of strategies for effective clinical management. Here, we summarize current knowledge about the molecular structure and biological function of Nrf2, and we discuss the roles of Nrf2 in tumorigenesis, which will further provide a possible therapeutic strategy for NSCLC.
Insights
Nuclear factor erythroid 2-related factor 2 (Nrf2) is crucial in non-small cell lung cancer (NSCLC) development and chemotherapy resistance. Understanding Nrf2
Area of Science:
- Molecular Biology
- Oncology
- Cellular Signaling
Background:
- The Keap1/Nrf2 pathway regulates gene expression and protein degradation.
- Aberrant Keap1/Nrf2 signaling is implicated in non-small cell lung cancer (NSCLC) pathogenesis.
- High Nrf2 expression and low Keap1 levels correlate with poor NSCLC prognosis.
Purpose of the Study:
- To elucidate the molecular structure and biological functions of Nrf2.
- To discuss the role of Nrf2 in NSCLC tumorigenesis.
- To explore potential therapeutic strategies targeting Nrf2 in NSCLC.
Main Methods:
- Literature review and synthesis of current knowledge on Nrf2.
- Analysis of the Keap1/Nrf2 pathway in the context of NSCLC.
- Discussion of Nrf2's involvement in tumorigenesis and therapeutic implications.
Main Results:
- Nrf2 acts as a key transcription factor regulating downstream genes.
- Keap1 negatively regulates Nrf2 via proteasomal degradation.
- Dysregulation of the Keap1/Nrf2 pathway contributes to NSCLC progression and chemoresistance.
Conclusions:
- Understanding Nrf2's role is essential for NSCLC tumorigenesis.
- Targeting the Nrf2 pathway may offer novel therapeutic strategies for NSCLC.
- Further research into Nrf2 mechanisms can improve clinical management of NSCLC.
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