ArticleDrug design, development and therapy2025
Mechanistic Exploration of Shugan Jianpi Formula for Treating Triple-Negative Breast Cancer Under Chronic Stress: A Network Pharmacology-Guided Experimental Study.
Article in Drug design, development and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- Chronic psychosocial stress: a role in breast cancer etiology?Frontiers in oncology · 2026Pooled it
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: This study aimed to investigate the pharmacological mechanisms of Shugan Jianpi Formula (SGJPF) in treating TNBC using network pharmacology and molecular biology approaches. Methods: HPLC/MS identified the key compounds in SGJPF. In vitro assays were performed on norepinephrine (NE)-stimulated MDA-MB-231 and SUM159PT cells to mimic triple-negative breast cancer (TNBC) under chronic psychological stress (CPS) and evaluate SGJPF's effects on cell proliferation, apoptosis, cell cycle, migration, and invasion. A TNBC mouse model exposed to CPS was used to assess SGJPF's influence on tumor growth. SGJPF's mechanisms were explored via network pharmacology and molecular docking, with target validation through Western blotting, immunohistochemistry, and immunofluorescence. Results: HPLC/MS analysis identified 806 compounds in SGJPF, including flavonoids, polyphenols, saponins, polysaccharides, alkaloids, terpenoids, coumarins, organic acids, and glycosides. Network pharmacology and molecular docking analyses identified SRC, ERK (MAPK1), and STAT3 as pivotal targets underlying the anti-tumor effects of SGJPF in TNBC. Both in vitro and in vivo experiments confirmed that SGJPF exerts its therapeutic effects through the modulation of the SRC/ERK/STAT3 signaling axis. In vitro, SGJPF effectively inhibited TNBC cell proliferation, migration, and invasion, while promoting apoptosis in NE-stimulated cells. In a CPS-induced TNBC mouse model, SGJPF significantly alleviated tumor progression, further corroborating its potential as a novel therapeutic strategy for TNBC. Conclusion: This study highlights the potential of SGJPF as a therapeutic strategy for TNBC through its modulation of the SRC/ERK/STAT3 signaling axis, offering a robust foundation for further investigation into its clinical application.
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Registered trials
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