ArticleCancer research2026
Cancer Susceptibility to Stapled Oncolytic Peptides Is Dictated by Membrane Cholesterol and Inflammatory Signaling.
Article in Cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
Relapsed and refractory cancers effectively overcome diverse treatment modalities that primarily target nucleic acids and proteins. The plasma membranes of cancer cells represent an alternative and underutilized target, with the potential for membrane lysis to induce rapid, proinflammatory cell death that circumvents the challenges of intratumor heterogeneity and immune evasion. In this study, we repurposed StAMP51.2, a stapled magainin 2 peptide previously optimized for selective membrane lysis of Gram-negative bacteria, to target cancer cell membranes. The Profiling Relative Inhibition Simultaneously in Mixtures (PRISM) assay, a high-throughput cancer cytotoxicity screen, revealed cancer cells most vulnerable to StAMP51.2 and biomarkers of susceptibility, specifically reduced cholesteryl esters and elevated triacylglycerols. This signature was validated in pairs of sensitive (OCI-AML3 and THP-1) and resistant (K562 and KMS-11) leukemia cell lines, with their differential responses correlated to distinct lipidomic profiles. Susceptibility of OCI-AML3 cells in culture extended to the in vivo context, in which StAMP51.2 suppressed leukemic growth in orthotopic and intraperitoneal models. To further characterize the mechanism of action, StAMP51.2-resistant OCI-AML3 cells were generated, which required 4 months of low-level exposure. Strikingly, drug-resistant OCI-AML3 cells recapitulated the lipidomic phenotype of naturally resistant K562 cells. Transcriptomic analyses further revealed that lipid reprogramming was accompanied by pervasive downregulation of inflammatory signaling. Thus, in advancing StAMP51.2 as an oncolytic prototype, this study uncovered an immunoregulatory axis that links membrane integrity to inflammatory signaling. SIGNIFICANCE: A stapled oncolytic peptide targets cancer cell membranes and induces a lipid-inflammation axis that underlies susceptibility, offering a promising therapeutic strategy beyond traditional nucleic acid and protein targets.
Indexed as
Identifiers
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.