ArticleDrug design, development and therapy2025
FAK-Induced Time Dependent Cell Response Profiling: Prediction, Identification, and Analysis of Anti-Tumor Immune Natural Products.
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 2 papers.
What it found
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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
2 citing papers in PubMed.
- New indole-linked 1,2,4-triazole derivatives as dual FAK inhibitors and apoptosis inducers targeting survival and migration in triple-negative breast cancer in-vitro.Scientific reports · 2026Article
- Unlocking Lung Cancer Cell Dormancy: An Epigenetic Perspective.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Focal Adhesion Kinase (FAK) is a key tyrosine kinase often overexpressed in tumors, making it a promising target for cancer therapy. This study aims to screen and investigate the activity and mechanisms of Traditional Chinese Medicines (TCMs) targeting FAK within breast cancer. Materials and Methods: Using xCELLigence system, we identified TCMs affecting FAK signaling and validated its anti-tumor effects. The 4T1-Luc breast cancer models and MMTV-PyMT mice were used to evaluate Results: We have successfully developed the EGF-induced Time-dependent Cell Response Profilings (FAK-TCRPs) and discovered that MCR effectively attenuated EGF-mediated responses in a dose-dependent manner. Additionally, MCR significantly inhibited tumor growth and lung metastasis by partly targeting FAK. MCR increased CD8 Conclusion: Collectively, MCR is identified as a FAK-targeting agent through FAK-TCRPs. MCR inhibits TAMs, CTLA-4, and chemokine transcription via the FAK/MMPs pathway, showing antitumor effects in breast cancer.
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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 OpenQuestion graph.