Yazar "Da'i, Muhammad" seçeneğine göre listele

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    Characterization of Zerumbone Loaded Chitosan-Folic Acid Nanoparticles and Its Cytotoxic Activity Against MCF-7 Cells
    (AMG Transcend Association, 2024) Trisakti, Intan; Da'i, Muhammad; Wikantyasning, Erindyah Retno; Mirzaei, Mahmoud
    Zerumbone has the potential to be developed as an anticancer because it has a variety of effects on the proliferation, angiogenesis, and apoptosis of different cancer cell lines. Because of the well-known folate-receptor mediated endocytosis, folic acid-chitosan conjugated nanoparticles demonstrated much greater cell uptake capacity. Zerumbone will be described after being formed into a nanoparticle system using a chitosan carrier conjugated with folic acid, compared to zerumbone-loaded chitosan nanoparticles. Employing the MTT assay method, nanoparticles were prepared by ionic gelation and characterized based on particle size, polydispersity index, zeta potential, entrapment efficiency, drug loading, release test, and cytotoxic test MCF7 cells. The synthesized nanoparticles had a zeta potential of-37.06, a PDI value of 0.32, and an average particle size of 195.13 nm. The percentage of nanoparticles released in 24 hours was 10.35%, while the %EE values were 74.96 % and %DL 15.23 %. The IC50 value of zerumbone chitosan-folic acid nanoparticles was 14.270 µg/ml. Zerumbone chitosan-folic acid nanoparticles were successfully synthesized using the ionic gelation method, well characterized, and showed cytotoxicity toward MCF7 cells. © 2024 by the authors.
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    Öğe
    Screening and identification of potential target of 1′-acetoxychavicol acetate (ACA) in acquired lapatinib-resistant breast cancer
    (Elsevier Ltd, 2024) Wulandari, Febri; Fauzi, Ahmad; Da'i, Muhammad; Mirzaei, Mahmoud; Maryati; Harismah, Kun
    1′-Acetoxychavicol acetate (ACA) eliminates breast cancer cells via the HER2/MAPK/ERK1/2 and PI3K/AKT pathways, and it also directly influences endocrine resistance by both enhancing pro-apoptotic signals and suppressing pro-survival molecules. This study utilized bioinformatics to assess ACA target genes for lapatinib-resistant breast cancer. We identified differentially expressed genes (DEGs) using GSE16179 microarray data. DEGs from ACA-treated and lapatinib-resistant cells were analyses using Panther DB, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses, and protein-protein interaction (PPI) network analysis. Genomic mutations, expression levels, prognostic significance, and ROC analysis were examined in selected genes. We used AutoDock Vina to conduct ACA molecular docking with potential target genes. In the PPI network analysis, BCL2, CXCR2, and CDC42 were the three highest-scoring genes. Genetic modification analysis identified PLAU and SSTR3 as the genes most frequently altered in breast cancer samples. The RTK-Ras pathway is likely to be affected by changes in BCL2, CXCR2, CDC42, SSTR3, PLAU, ICAM1, IGF1R, and MET genes. Patients with breast cancer who had lower levels of BCL2, SSTR3, PLAU, ICAM1, IGF1R, and MET had worse overall survival compared to other groups. ACA exhibited moderate binding affinity to BCL2, SSTR3, PLAU, ICAM1, IGF1R, and MET. Overall, ACA might counteract breast cancer resistance to lapatinib by targeting BCL2, SSTR3, PLAU, ICAM1, IGF1R, and MET. Further in vitro studies involving gene silencing could provide more detailed insights into the mechanism by which ACA combats lapatinib resistance. © 2024