NRF1 Regulates the Epithelial Mesenchymal Transition of Breast Cancer by Modulating ROS Homeostasis

Author:

Sun Linjuan12,Ouyang Nan12,Shafi Shaheryar12ORCID,Zhao Rongchuan12,Pan Jinlin12,Hong Lei12,Song Xueyan2,Sa Xiaohan12,Zhou Yuanshuai12ORCID

Affiliation:

1. School of Biomedical Engineering (Suzhou), University of Science and Technology of China, Hefei, China

2. Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Sciences, Suzhou, China

Abstract

Introduction: Nuclear respiratory factor 1 (NRF1) is an important regulator involved in mitochondrial biogenesis and energy metabolism. However, the specific mechanism of NRF1 in anoikis and epithelial-mesenchymal transition (EMT) remains unclear. Methods: We examined the effect of NRF1 on mitochondria and identified the specific mechanism through transcriptome sequencing, and explored the relationships among NRF1, anoikis, and EMT. Results: We found that upregulated NRF1 expression led to increased mitochondrial oxidative phosphorylation (OXPHOS) and ATP generation. Simultaneously, a significant amount of ROS is generated during OXPHOS. Alternatively, NRF1 upregulates the expression of ROS-scavenging enzymes, allowing tumor cells to maintain low ROS levels and promoting anoikis resistance and EMT. We also found that exogenous ROS was maintained at a low level by NRF1 in breast cancer cells. Conclusion: our study provides mechanistic insight into the function of NRF1 in breast cancer, indicating that NRF1 may serve as a therapeutic target for breast cancer treatment.

Funder

National Natural Science Foundation of China

Publisher

SAGE Publications

Subject

Cancer Research,Oncology

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