ArticleCancer biology & therapy2024
NRF3 suppresses the malignant progression of TNBC by promoting M1 polarization of macrophages via ROS/HMGB1 axis.
Article in Cancer biology & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Integrating single-cell RNA and bulk RNA sequencing data to identify prognostic genes associated with pyrimidine metabolism in triple-negative breast cancer by machine learning algorithm combinations.Discover oncology · 2026Article
- Nrf3: an emerging player in cancer, inflammation, and cellular homeostasis.Molecular biology reports · 2026Review
- A comprehensive review of the emerging role of NRF3 in ovarian cancer tumorigenesis and progression.Journal of ovarian research · 2026Review
- Treatment strategies targeting the phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin pathway against triple-negative breast cancer.World journal of clinical oncology · 2025Review
- Molecular mechanisms and pathological implications of unconventional protein secretion in human disease: from cellular stress to therapeutic targeting.Molecular biology reports · 2025Review
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5 authors.
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Abstract
backgroundTriple-negative breast cancer (TNBC) is a highly aggressive form of breast cancer. Due to its lack of targeted therapy options, TNBC remains a significant clinical challenge. In this study, we investigated the role of nuclear respiratory factor 3 (NRF3) and high-mobility group box 1 (HMGB1) in the progression of TNBC.
methodsThe study analyzed NRF3's clinical expression, differentially expressed genes (DEGs), and immune infiltration in TNBC using the TCGA database and bioinformatics tools. Cellular functions of MDA-MB-468 and Hs578t cells were evaluated through MTT, colony formation, transwell, flow cytometry, and western blotting. The regulatory function of NRF3 in TNBC cell lines was assessed using Immunofluorescence, Immunohistochemistry, qRT-PCR, CHIP, luciferase assay, and ELISA. Moreover, a xenograft model was established to investigate the role of NRF3 in TNBC in vivo.
resultsLow expression of NRF3 in TNBC tumors was associated with unfavorable prognosis and transcripts from tumors with higher NRF3 levels were enriched in oxidative stress and immune-related pathways. The subsequent gain- and loss-functional experiments indicated that NRF3 overexpression significantly suppressed malignant phenotypes, MAPK/ERK signaling pathways, and epithelial-mesenchymal transition (EMT), whereas it promoted reactive oxygen species (ROS) levels in TNBC. Further mechanistic exploration showed that NRF3 inhibited TNBC cell function by regulating oxidative stress-related genes to inhibit the MAPK/ERK signaling pathway by promoting the release of HMGB1 via ROS, thereby promoting M1 macrophage polarization.
conclusionNRF3 promotes M1 macrophage polarization through the ROS/HMGB1 axis, thereby inhibiting the malignant progression of TNBC. It is expected to become a therapeutic biomarker for TNBC.
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