ArticleScientific reports2025
Repurposing cephalosporins as excellent anticancer agents and chemosensitizers for inflammation-driven cancer therapy.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
- Erratum issued
Authors and funding
15 authors.
Funding
Abstract
Could cephalosporin antibiotics, extending beyond their established antimicrobial role, be repurposed as precision anticancer agents and chemosensitizers, particularly against inflammation-driven carcinogenesis? To address this question, this study systematically evaluated the anti-colorectal cancer efficacy of cephalosporins both as monotherapies and in synergistic combinations, elucidating their underlying molecular mechanisms. Employing combinatorial phenotypic screening (viability, cell cycle, apoptosis, colony formation), BALB/c nude mouse xenografts, and omics profiling (RNA-seq, RT-qPCR), we identified conserved anticancer pathways and core regulatory axes. Among 18 evaluated cephalosporins, therapeutic specificity was largely associated exclusively variable side-chain moieties, not the conserved β-lactam core. Cefamandole nafate (CAN) and cefuroxime sodium (CUS) demonstrated potent dual efficacy against colorectal cancer model while enhancing cisplatin chemosensitivity. Building on links to inflammation-driven chemosensitization, CUS synergistically potentiated cisplatin and levofloxacin cytotoxicity in colorectal cancer. This synergy was mechanistically driven by apoptosis induction, cell cycle arrest, significant up-regulation of HMOX1 (80-fold peak in combinations; 40-fold as monotherapy) and DDIT3, coupled with down-regulation of MUC1, CASC19, KRT23, SPNS3, LFNG, HS3ST1, NCOA5, and GJB4. Crucially, we reveal for the first time that CUS significantly up-regulates HMOX1 expression in HCT116 cells in a dose-dependent manner, establishing this ferroptosis regulator as the central effector governing both intrinsic anticancer activity and chemosensitization. This study unveils the translational potential of repurposing cephalosporins for combinatorial precision oncology strategies targeting inflammation-driven cancers.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.