ArticleScientific reports2025
In silico approaches unveil the mechanism of action of Eclipta prostrata against acute myeloid leukemia.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed.
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- Review
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- Computational discovery of marine natural phytochemicals as novel SIRT7 inhibitors for cancer treatment.Journal, genetic engineering & biotechnology · 2026Article
- In silico evaluation of garlic-derived organosulfur compounds as multi-target inhibitors of breast cancer biomarkers.PloS one · 2026Article
- Computational screening of oncogenic genetic variations in tumor suppressor proteins driving gastric cancer pathogenesis.PloS one · 2026Article
- Transcriptomics analysis unveils the complex interplay between diabetes and hypertension in regulating renal cell carcinoma pathway followed by pancreatic metastasis.Journal, genetic engineering & biotechnology · 2025Article
- Screening the Active Phytochemicals FromCancer innovation · 2025Review
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11 authors.
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Abstract
Acute myeloid leukemia (AML) is an aggressive hematological malignancy with a poor prognosis. While the medicinal plant Eclipta prostrata has shown promising anticancer properties against AML, its underlying mechanisms against AML remain largely unexplored. Hence, this study aimed to unveil the molecular mechanisms of E. prostrata, identify therapeutic targets, detect regulatory elements, and discover potential biomarkers for AML using comprehensive in-silico analyses. We implemented an integrated computational approach combining network pharmacology, molecular docking, molecular dynamics simulations, 3D-QSAR modeling, gene regulatory network, gene expression, patient survival, and cancer hallmarks analysis to investigate the mechanism of action of E. prostrata against AML. Our computational approaches identified 12 potential anti-cancer compounds from E. prostrata. Molecular docking revealed strong binding affinities of Kaempferol (-8.931 kcal/mol) and Apigenin (-8.752 kcal/mol) to FLT3, compared to control Pacritinib (-5.403 kcal/mol). Tricetin (-8.634 kcal/mol) and Diosmetin (-7.780 kcal/mol) showed strong binding to PIM1 compared to control SEL24 (-6.385 kcal/mol). Post-molecular dynamics simulation MM-GBSA analysis further confirmed these interactions, with binding free energies for FLT3: Kaempferol (-73.75 kcal/mol), Apigenin (-68.76 kcal/mol), Pacritinib (-51.27 kcal/mol); and for PIM1: Tricetin (-64.28 kcal/mol), Diosmetin (-52.2 kcal/mol), SEL24 (-53.38 kcal/mol). Predicted IC
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