ArticleCell biochemistry and biophysics2026
Computational Design Of A Peptide Candidate Targeting NOTCH1 And PI3K/AKT Signaling Pathways In Cancer: A Coarse-Grained Molecular Dynamics Simulation Study.
Article in Cell biochemistry and biophysics, 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The PI3K/AKT and NOTCH1 signaling pathways are key regulators of tumor progression, proliferation, survival, and metastasis in numerous cancers, making them attractive targets for peptide-based anticancer therapies. Dermaseptin-B2 is a well-characterized anticancer peptide known to modulate the PI3K/AKT signaling pathway; however, its therapeutic application may be limited by suboptimal cellular uptake. In contrast, Magainin-2 exhibits strong membrane-interacting and cell-penetrating properties and has been widely employed in the development of hybrid bioactive peptides to enhance membrane permeability and intracellular delivery. In this study, a peptide library was constructed from truncated fragments of Dermaseptin-B2 and Magainin-2 to identify hybrid peptides targeting the PI3K/AKT and NOTCH1 signaling pathways. A five-amino-acid anticancer motif derived from Dermaseptin-B2 was fused to a ten-amino-acid membrane-active fragment of Magainin-2 to improve cellular penetration. Subsequently, three rational amino acid substitutions were introduced into the lead peptide (MD3)-lysine replacing phenylalanine, histidine replacing glycine, and valine replacing serine-to enhance anticancer activity, optimize cell penetration, and reduce potential toxicity. Molecular docking analyses demonstrated favorable binding of MD3 to proteins involved in the PI3K/AKT and NOTCH1 signaling pathways. Molecular dynamics simulations, including RMSD, RMSF, and radius of gyration analyses, confirmed the structural stability of the peptide-protein complexes throughout the simulation period. Binding free-energy calculations using the MM-PBSA method indicated thermodynamically favorable interactions between MD3 and its target proteins. Furthermore, analyses of hydrogen-bond distance and angle distributions supported the formation of stable, geometrically favorable intermolecular interactions. Coarse-grained membrane simulations further demonstrated the efficient membrane-penetrating capability of MD3 in a DOPS-DOPC lipid bilayer model. Collectively, these findings identify MD3 as a promising multifunctional hybrid peptide that targets multiple cancer-associated signaling pathways and exhibits favorable membrane penetration and structural stability, highlighting its potential as a candidate for future peptide-based anticancer therapeutics.
Indexed as
Identifiers
42776373What 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.