ArticleFrontiers in pharmacology2026
Integrative analysis of
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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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.
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Triple-negative breast cancer (TNBC) urgently needs effective therapies due to limited targeted options and unfavorable outcomes. We investigated Methods: Liquid chromatography coupled with mass spectrometry was employed to identify the components of TKM formula granules. Network pharmacology-based prediction was used to uncover potential mechanisms by which TKM counteracts TNBC. Potential targets were identified, and pathway enrichment analysis was performed. Subsequently, TNBC cells and 4T1 tumor-bearing mice were used to verify the molecular mechanisms of TKM. Results: We identified 151 active compounds in TKM. Through network pharmacology analysis, 214 TNBC-related targets were found, with 28 core targets, including cell cycle and apoptosis regulators MYC, TP53, AKT1, CCND1, CASP3, PIK3CA, BCL2L1, and CDC42. The compound-target-pathway-disease network showed that schisandrin binds to many treatment targets with satisfactory docking performance, especially for MYC and AKT1. Experimentally, TKM was found to significantly promote apoptosis and induce G2/M-phase cell-cycle arrest in MDA-MB-231 cells. Western blot analysis showed that TKM suppressed PI3K/AKT and Wnt/β-catenin signaling pathways. Surface plasmon resonance experiment revealed that schisandrin binds to recombinant AKT1 with an equilibrium dissociation constant (K_D) of 1.525 × 10 Conclusion: This study comprehensively explores the multi-target mechanisms of TKM against TNBC using network pharmacology, molecular pharmacology, and metabolomics approaches. These findings provide a foundation for future mechanistic investigations and may support the further preclinical development of TKM-based strategies for TNBC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.