ArticleBMC pharmacology & toxicology2026
Synergistic combination of pirfenidone and paclitaxel suppresses migration and stemness in triple-negative breast cancer: implications of EMT and pluripotency pathways.
Article in BMC pharmacology & toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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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
1 citing paper in PubMed.
- Hallmarks of epithelial-mesenchymal plasticity in cancer.Molecular cancer · 2026Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) is an aggressive type of cancer with limited treatment options and high risks of metastasis and recurrence. Growing evidence shows that paclitaxel (PTX), a first-line chemotherapeutic agent in TNBC, may paradoxically promote pro-metastatic features of epithelial-mesenchymal transition (EMT) and cancer stemness in surviving cancer cells. The present study investigated the potential of pirfenidone (PFD), an anti-fibrotic drug, in combination with PTX against cancer proliferation, migration, and stemness of MDA-MB-231 cells. Findings by CompuSyn demonstrated strong synergism between PTX and PFD (combination index < 1), allowing significant reductions in doses. Indeed, the IC50 value of the PTX + PFD combination was found to be 2.02 µg/ml + 348.954 µg/ml, which, compared to the IC50 values of each drug alone, underwent a significant reduction from 5.54468 µg/ml to 2.02 µg/ml for PTX and from 952.633 µg/ml to 348.954 µg/ml for PFD, which were below half of each drug’s IC50. The combination also induced higher apoptotic rates in comparison to monotherapies. While PTX monotherapy led to up-regulation of the EMT transcription factor Twist, the PTX + PFD combination strongly led to suppression of key EMT markers, including Twist, Snail, and N-cadherin, and further inhibited cell migration. Moreover, the combination efficiently targeted cancer stemness, as evidenced by a reduction in colony-forming capability and the downregulation of pluripotency transcription factors, including NANOG, OCT-4, and SOX2. Our findings demonstrated that not only did PFD show synergistic effects along with PTX to improve cytotoxicity, but it was also associated with considerably mitigated PTX-induced pro-metastatic and stem-like characteristics. Therefore, repurposing PFD alongside PTX may offer a promising strategy to synergistically enhance antitumor efficacy while mitigating therapy-induced pro-metastatic pathways in TNBC.
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