ArticleOncology letters2025
ERK-driven autophagy enhances synergy of eribulin and cisplatin in triple-negative breast cancer.
Article in Oncology letters, 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.
- Does coordinated targeting of metabolism and autophagy, modulated by microtubule dynamics, influence therapeutic vulnerability to eribulin in glioblastoma?Translational cancer research · 2026Article
- Mesenchymal stem cells promote cisplatin resistance in non-small cell lung cancer through IL-6/MEK-ERK/macrophages axis: construction of prognostic signature and experimental investigation.Frontiers in pharmacology · 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) remains one of the most aggressive subtypes of breast cancer with limited therapeutic options, especially in resource-limited settings. The present study investigated the mechanistic synergy of eribulin and cisplatin in TNBC, with a focus on ERK-driven autophagy. MDA-MB-231 TNBC cells were treated with eribulin and cisplatin. Viability, apoptosis, autophagy and ERK activation were assessed using Cell Counting Kit-8 assays, flow cytometry, western blotting and fluorescence microscopy. The drug combination enhanced ERK activation and induced autophagy, significantly increasing cell death. ERK inhibition reversed these effects, confirming its role in mediating synergy. The present findings provide a mechanistic rationale for an affordable combination therapy that may enhance TNBC treatment efficacy, particularly in resource-limited settings.
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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.