ReviewInternational journal of molecular sciences2025
Autophagy-Related Proteins in Triple-Negative Breast Cancer: From Molecular Insights to Therapeutic Applications.
Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
5 citing papers in PubMed.
- Nanoparticle-Mediated TIPE1 mRNA Delivery Enhances Paclitaxel Sensitivity in Triple-Negative Breast Cancer by Modulating RAB7A Ubiquitination-Associated Stability and Autophagy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Breast Cancer: Epidemiology, Molecular Classification, Diagnostics and Evolving Treatment Paradigms.Molecules (Basel, Switzerland) · 2026Review
- Targeting Autophagy to Overcome Chemoresistance and Immune Resistance in Triple-Negative Breast Cancer.Cancers · 2026Review
- Punicalin Modulates Angiogenesis and Tumor Microenvironment-Related Processes in Triple-Negative Breast Cancer and Endothelial Cells.International journal of molecular sciences · 2026Article
- The Landscape of Ferroptosis-Related Gene Signatures as Molecular Stratification in Triple-Negative Breast Cancer.Diagnostics (Basel, Switzerland) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) represents the most aggressive and therapeutically recalcitrant breast cancer subtype, exhibiting dismal clinical outcomes due to its intrinsic heterogeneity and lack of molecularly targeted treatment options. Emerging evidence has established the autophagy-related proteins (ARPs) as key regulators of TNBC pathogenesis, functioning not only as metabolic gatekeepers but also as multifaceted modulators of malignant transformation, disease progression, and therapeutic responsiveness. These proteins exert diverse functions in TNBC through both canonical autophagy-dependent pathways and non-canonical mechanisms. In this review, we critically examine the pleiotropic functions and molecular mechanisms of ARPs in TNBC progression and therapeutic responsiveness, with special emphasis on their context-dependent roles in both fortifying therapeutic resistance and, paradoxically, creating vulnerabilities for therapeutic exploitation.
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What Socratic holds
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.