ArticleActa pharmaceutica Sinica. B2025
Psychological stress-activated NR3C1/NUPR1 axis promotes ovarian tumor metastasis.
Article in Acta pharmaceutica Sinica. B, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Mechanisms of Paclitaxel Resistance: Recent Advances and Future Perspectives.International journal of molecular sciences · 2026Review
- Depression remodels tumor microenvironment to drive tumor progression: Bio-behavioural signalling pathways and clinical interventions.Journal of advanced research · 2026Review
- Targeting the NR3C1-ACSL4 Axis Triggers Ferroptosis to Overcome Radioresistance in Prostate Cancer.Cancer science · 2026Article
- Laser microdissection-based multi-omics integration unveils the pathological atlas and tumor differentiation network of adamantinomatous craniopharyngioma.Acta neuropathologica communications · 2026Article
- NR3C1 Modulates Wnt Signalling to Influence the Invasiveness and Immune Features of Nonfunctioning Invasive Pituitary Adenomas.Journal of cellular and molecular medicine · 2026Article
- Targeting glucocorticoid receptor signaling in platinum-resistant ovarian cancer: translational rationale and clinical advances following the ROSELLA trial.Oncology reviews · 2026Review
- The prognostic marker NRIP1 is associated with tumor progression and immune infiltration in acute myeloid leukemia.Acta biochimica et biophysica Sinica · 2025Article
- Fedratinib inhibits ovarian cancer progression by downregulating QPCT expression.Discover oncology · 2025Article
- Transformer-based classification and interpretability of NR3C1 expression patterns in OSCC: Metabolic adaptation insights.Journal of oral biology and craniofacial researchArticle
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16 authors.
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Abstract
Ovarian tumor (OT) is the most lethal form of gynecologic malignancy, with minimal improvements in patient outcomes over the past several decades. Metastasis is the leading cause of ovarian cancer-related deaths, yet the underlying mechanisms remain poorly understood. Psychological stress is known to activate the glucocorticoid receptor (NR3C1), a factor associated with poor prognosis in OT patients. However, the precise mechanisms linking NR3C1 signaling and metastasis have yet to be fully elucidated. In this study, we demonstrate that chronic restraint stress accelerates epithelial-mesenchymal transition (EMT) and metastasis in OT through an NR3C1-dependent mechanism involving nuclear protein 1 (NUPR1). Mechanistically, NR3C1 directly regulates the transcription of NUPR1, which in turn increases the expression of snail family transcriptional repressor 2 (SNAI2), a key driver of EMT. Clinically, elevated NR3C1 positively correlates with NUPR1 expression in OT patients, and both are positively associated with poorer prognosis. Overall, our study identified the NR3C1/NUPR1 axis as a critical regulatory pathway in psychological stress-induced OT metastasis, suggesting a potential therapeutic target for intervention in OT metastasis.
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