Evidence map›Paper›PMID 41721902›Full record

ArticleMolecular biology reports2026

Comparative multi-pathway inhibition of breast cancer by micro-and nano-formulated Curcumin.

Mahmoud Moawad, Afaf Altrawy, Ghada M Nasr, Wael S Abd El Aal, Mohamed Y Nasr, Mohab S Eissa, Emad S Shaker

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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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.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Mahmoud MoawadDepartment of Pathology, National Cancer Institute, Cairo University, Cairo, Egypt.
Afaf AltrawyDepartment of Medical Biotechnology, College of Biotechnology, Misr University for Science and Technology, P. O. Box 77, Giza, Egypt. Afaf.altrawy@must.edu.eg.ORCID http://orcid.org/0000-0001-9736-6401
Ghada M NasrFaculty of Biotechnology (Ex. GEBRI), Department of Molecular Diagnostics, University of Sadat City, Sadat, Egypt.
Wael S Abd El AalFaculty of Biotechnology (Ex. GEBRI), Department of Molecular Diagnostics, University of Sadat City, Sadat, Egypt.
Mohamed Y NasrFaculty of Biotechnology (Ex. GEBRI), Department of Molecular Biology, University of Sadat City, Sadat, Egypt.
Mohab S EissaDepartment of Pathology, National Cancer Institute, Cairo University, Cairo, Egypt.
Emad S ShakerFaculty of Agriculture, Biochemistry Dept, Minia University, Minya, Egypt.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

OBJECTIVES AND

backgroundBreast cancer (BC) remains a leading cause of cancer-related death among women. There is an urgent need for new therapies with fewer side effects. This study evaluated the anticancer potential of curcumin micro- and nanocapsules on MCF-7 breast cancer cells and explored the underlying molecular mechanisms using bioinformatics analysis. MATERIALS AND

methodsCurcumin micro- and nanocapsules were produced through mechanical encapsulation and tested on MCF-7 cells. Cell viability was measured by MTT assay, apoptosis and cell cycle changes were analyzed by flow cytometry, and gene expression of C-myc, Ki-67, EGFR, VEGFR2, and Caspase-3 was evaluated by real-time PCR. Public datasets (TCGA and CPTAC) were analyzed to identify curcumin-related genes, pathways, and drug-target networks.

resultsBoth formulations reduced cell viability by 45-60% and significantly increased apoptosis, with nanocapsules being more potent. Nanocapsules caused G2/M phase arrest and a 3.8-fold rise in Caspase-3 expression, while microcapsules mainly induced G0/G1 arrest. Treatments suppressed the proliferation markers C-myc and Ki-67, along with EGFR and VEGFR2. Bioinformatics analysis confirmed that these genes are key regulators in MAPK, PI3K/Akt, WNT, and HER2 pathways affected by curcumin.

conclusionNano-formulated curcumin demonstrates strong, multi-target anticancer activity by blocking cell growth and angiogenesis while promoting apoptosis. These findings support its potential as a safe and effective therapeutic option for breast cancer.

Indexed as

Breast NeoplasmsCurcuminAntineoplastic AgentsApoptosisCaspase 3Cell CycleCell ProliferationCell SurvivalErbB ReceptorsFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsNanocapsulesSignal TransductionVascular Endothelial Growth Factor Receptor-2Antineoplastic AgentsCaspase 3CurcuminErbB ReceptorsNanocapsulesVascular Endothelial Growth Factor Receptor-2ApoptosisCaspase3C-mycCurcumin microcapsulesEGFRIC50Ki-67MCF7 cell lineNanocapsulesVEGFR2

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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.