Screening and identification of potential target of 1′-acetoxychavicol acetate (ACA) in acquired lapatinib-resistant breast cancer

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dc.contributor.authorWulandari, Febri
dc.contributor.authorFauzi, Ahmad
dc.contributor.authorDa'i, Muhammad
dc.contributor.authorMirzaei, Mahmoud
dc.contributor.authorMaryati
dc.contributor.authorHarismah, Kun
dc.date.accessioned2025-03-17T12:22:45Z
dc.date.available2025-03-17T12:22:45Z
dc.date.issued2024
dc.departmentTarsus Üniversitesi
dc.description.abstract1′-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
dc.description.sponsorshipUniversitas Muhammadiyah Surakarta, UMS, (303.28/A.3- III / LRI /X/2023)
dc.description.sponsorshipUniversitas Muhammadiyah Surakarta, UMS
dc.identifier.doi10.1016/j.heliyon.2024.e40769
dc.identifier.issn2405-8440
dc.identifier.issue23
dc.identifier.scopus2-s2.0-85210679063
dc.identifier.scopusqualityQ1
dc.identifier.urihttps://doi.org/10.1016/j.heliyon.2024.e40769
dc.identifier.urihttps://hdl.handle.net/20.500.13099/1360
dc.identifier.volume10
dc.indekslendigikaynakScopus
dc.language.isoen
dc.publisherElsevier Ltd
dc.relation.ispartofHeliyon
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_Scopus_20250316
dc.subject1′-acetoxychavicol acetate
dc.subjectBioinformatics
dc.subjectBreast cancer
dc.subjectLapatinib-resistant
dc.subjectTargeted therapy
dc.titleScreening and identification of potential target of 1′-acetoxychavicol acetate (ACA) in acquired lapatinib-resistant breast cancer
dc.typeArticle

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