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Updated: Aug 5, 2025

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
NRF1 Regulates the Epithelial Mesenchymal Transition of Breast Cancer by Modulating ROS Homeostasis.
Linjuan Sun1,2, Nan Ouyang1,2, Shaheryar Shafi1,2
1School of Biomedical Engineering (Suzhou), 12652University of Science and Technology of China, Hefei, China.
Nuclear respiratory factor 1 (NRF1) promotes cancer cell survival by enhancing mitochondrial function and regulating reactive oxygen species (ROS) levels, thereby resisting anoikis and driving epithelial-mesenchymal transition (EMT). This suggests NRF1 as a potential therapeutic target for breast cancer.
Area of Science:
- Cell Biology
- Molecular Biology
- Cancer Research
Background:
- Nuclear respiratory factor 1 (NRF1) is crucial for mitochondrial biogenesis and energy metabolism.
- The precise role of NRF1 in anoikis and epithelial-mesenchymal transition (EMT) is not fully understood.
Purpose of the Study:
- To elucidate the mechanism by which NRF1 influences anoikis and EMT.
- To investigate the relationship between NRF1, mitochondrial function, and reactive oxygen species (ROS) in cancer cells.
Main Methods:
- Transcriptome sequencing was employed to identify the molecular mechanisms.
- Mitochondrial function, including oxidative phosphorylation (OXPHOS) and ATP generation, was assessed.
- The impact of NRF1 on ROS levels and ROS-scavenging enzymes was examined.
Main Results:
- Upregulated NRF1 expression enhanced mitochondrial OXPHOS and ATP production.
- NRF1 influences ROS generation during OXPHOS and upregulates ROS-scavenging enzymes.
- NRF1 maintains low exogenous ROS levels, promoting anoikis resistance and EMT in breast cancer cells.
Conclusions:
- NRF1 plays a significant role in promoting anoikis resistance and EMT through modulation of mitochondrial activity and ROS homeostasis.
- NRF1 represents a potential therapeutic target for breast cancer treatment.
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