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Life sciences · Journal article
Translational Oncology · October 14, 2026
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Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer characterized by high molecular heterogeneity and a lack of effective targeted therapies. Increasing evidence indicates that metabolic reprogramming and redox homeostasis are critical determinants of TNBC progression; however, the transcriptional mechanisms linking these processes to mitochondrial function remain incompletely understood. In this study, integrative bioinformatics analyses identified nuclear receptor subfamily 3 group C member 2 (NR3C2) as a potential regulatory factor in TNBC. NR3C2 expression was significantly decreased in TNBC and was associated with patient prognosis. Functional assays demonstrated that NR3C2 overexpression markedly inhibited cell proliferation and migration in vitro and suppressed tumor growth and dissemination in zebrafish xenograft models. Mechanistically, RNA sequencing identified NDUFB3, an accessory subunit of mitochondrial complex I, as a downstream target of NR3C2. Dual-luciferase reporter assays further confirmed that NR3C2 directly regulates NDUFB3 transcription. Functional analyses revealed that NR3C2 modulates mitochondrial activity, as evidenced by increased mitochondrial membrane potential and complex I activity, accompanied by reduced ATP production and elevated reactive oxygen species (ROS) levels. Notably, NR3C2-induced ROS accumulation promoted apoptosis, whereas these effects were partially reversed by NDUFB3 knockdown or treatment with the ROS scavenger N-acetylcysteine (NAC). Consistently, in vivo experiments demonstrated that NR3C2 suppresses tumor growth and metastasis in a ROS-dependent manner. Collectively, these findings indicate that NR3C2 inhibits TNBC progression by regulating mitochondrial function and ROS homeostasis, at least in part through NDUFB3. This study provides new insights into the interplay between transcriptional regulation and mitochondrial redox balance and highlights NR3C2 as a potential therapeutic target for TNBC.