ArticleInternational journal of molecular sciences2025
Synergistic Effects of Oxaliplatin, 5-Fluorouracil, and Novel Synthetic Uracil Analog U-359 on Breast Cancer Cell Carcinogenesis.
Article 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 2 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
2 citing papers in PubMed.
- Chemotherapeutic Potential of Fluorouracil-Platinum (IV) Prodrugs Against Cisplatin-Resistant Colorectal Cancer Cells.Chemistry (Weinheim an der Bergstrasse, Germany) · 2026Article
- Special Issue "Molecular Research and Cellular Biology of Breast Cancer".International journal of molecular sciences · 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
Abstract
Breast cancer presents significant global challenges, necessitating effective treatments to combat drug resistance and minimize chemotherapy side effects. This study evaluated the cytotoxic effects of U-359, Oxaliplatin (Ox), and 5-Fluorouracil (5-FU) in MCF-7 and MCF-10A cells using MTT and RealTime-GLO assays. Morphological changes were assessed by light microscopy following Wright-Giemsa staining. Apoptosis induction was studied using qPCR for apoptotic markers, the RealTime-Glo™ Annexin V assay, and the cleaved PARP1 ELISA assay. Caspase 8 and 9 activities, ABCB1, ABCG2, and NF-κB protein levels were quantified using ELISA. Synergy was analyzed using the Bliss Independence Model. The results indicated that combining U-359 with Ox and 5-FU enhanced cytotoxicity compared to individual treatments. U-359 induced apoptosis-associated morphological changes in MCF-7 cells, which were augmented with the Ox and 5-FU treatment. Apoptosis assays confirmed the up-regulation of pro-apoptotic markers and the down-regulation of anti-apoptotic markers with U-359 alone or in combination. Elevated cleaved PARP1 levels suggested robust apoptosis induction with U-359 and Ox or 5-FU. Caspase activity assays demonstrated a significant activation of caspase 8 and 9, implicating both apoptotic pathways. Furthermore, U-359 down-regulated ABCB1, ABCG2, and NF-κB in MCF-7 cells, which were up-regulated by Ox and 5-FU alone. The Bliss Independence Model revealed strong synergistic interactions (SI < 1) between U-359 and Ox or 5-FU, particularly in reducing ABCB1 and NF-κB levels. U-359 combined with Ox and 5-FU shows potential for overcoming chemotherapy resistance in breast cancer by enhancing apoptosis and modulating drug resistance. Further clinical studies are needed to optimize treatment and improve outcomes.
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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.