ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Integrated computational and in vitro investigation to explore the preliminary anti-proliferative and anti-mitotic potential of γ-oryzanol against breast cancer.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study investigated the preliminary role of γ-oryzanol (γ-O) against breast cancer through computational and in vitro analyses. Reference protein set (RPS) and functional enrichment set (FES) proteins were identified and subjected to network pharmacology. Pharmacogenomics analysis assessed expression profiles and survival associations. Molecular docking of γ-O with PIK3CA, AKT1, AKR1C3, ESR1, and MAPK1 was performed, followed by molecular dynamics (MD) simulation of the γ-O-PIK3CA complex. Brine shrimp lethality assay (BSLA) evaluated the effect of γ-O on nauplii survival and percentage lethality. Allium cepa root tip assay (ACARTA) assessed the effect of γ-O in number and length of roots. Cell viability assay evaluated MCF-7 cell viability after γ-O treatment. Target validation and network pharmacology suggested the relevance of RPS and FES with cancer-associated pathways. Pharmacogenomics analysis highlighted FES overexpression with reduced survival associations and cancer progression. Molecular docking predicted interaction of γ-O with PIK3CA (- 9.1 kcal/mol), AKT1 (- 7.2 kcal/mol), AKR1C3 (- 12.3 kcal/mol), ESR1 (- 8.3 kcal/mol), and MAPK1 (- 8.9 kcal/mol). MD simulation indicated the stability of γ-O-PIK3CA complex. γ-O treatment significantly (P-value < 0.05) reduced nauplii survival and increased percentage lethality. The number and length of roots reduced significantly (P-value < 0.05) in γ-O-treated roots. γ-O produced a significant (P-value < 0.05) concentration-dependent reduction in cell viability (half-maximal inhibitory concentration = 352.57 ± 48.51 µg/mL). BSLA, ACRTA, and cell viability assay demonstrated preliminary cytotoxic, anti-mitotic, and anti-proliferative effects of γ-O, aligned with computational target and interaction analyses. Further studies are required to validate its mechanistic relevance against breast cancer.
Indexed as
Identifiers
42525294What 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.