ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Bufalin Inhibits the PI3K/AKT Pathway by Targeting GTF3C4 to Impede Breast Cancer Progression.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- Bufalin-Loaded Multifunctional Nanodrugs for Cancer Therapy: Mechanisms, Delivery Strategies, and Translational Perspectives.Biomolecules · 2026Review
- Acidosis-associated gene signature defines novel subtypes and dual-target therapeutic candidates in breast cancer.Journal of translational medicine · 2026Article
- Bufalin Suppresses Pancreatic Ductal Adenocarcinoma Through ER Stress-Ferroptosis Crosstalk Associated with IPInternational journal of molecular sciences · 2026Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Breast cancer incidence is rising globally, presenting challenges such as treatment side effects and drug resistance. Bufalin is a bufadienolides compound with potential anti-cancer effects. This study shows that bufalin inhibits malignant proliferation of MDA-MB-231 and MCF-7 cells and protects mice against breast cancer. Of note, GTF3C4 was identified as the target protein by Limited Proteolysis-Mass Spectrometry. GTF3C4 is overexpressed in breast cancer and associated with poor prognosis. RNA sequencing analysis reveals that the PI3K/AKT signaling pathway is a key contributor. Using cell thermal shift assays, drug affinity response target stability assays, and surface plasmon resonance, it was verified that bufalin can specifically bind to GTF3C4. Bufalin reduces GTF3C4 protein levels in vivo and in vitro, effectively inhibiting breast cancer progression by suppressing the PI3K/AKT signaling pathway. After the knockdown of GTF3C4, the PI3K/AKT signaling pathway is also suppressed, thereby inhibiting the proliferation of breast cancer cells and promoting apoptosis. Single-cell RNA sequencing results indicated that bufalin reduces the proportions of macrophages, neutrophils, and monocytes, and affects the strength of receptor-ligand signals between cells. Collectively, this study demonstrates that bufalin targets GTF3C4 to inhibit the PI3K/AKT pathway and remodels the tumor microenvironment, thereby hindering the malignant progression of 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.