Network and Computational Drug Repurposing Analysis for c-Myc Inhibition in Burkitt Lymphoma
- Authors
- LEE, YONGMIN; NAM, SEUNGYOON
- Issue Date
- Dec-2023
- Publisher
- International Institute of Anticancer Research
- Keywords
- Burkitt lymphoma; c-Myc; drug repurposing; vorinostat
- Citation
- Cancer Genomics and Proteomics, v.20, no.6, pp 712 - 722
- Pages
- 11
- Journal Title
- Cancer Genomics and Proteomics
- Volume
- 20
- Number
- 6
- Start Page
- 712
- End Page
- 722
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/90481
- DOI
- 10.21873/cgp.20418
- ISSN
- 1109-6535
1790-6245
- Abstract
- BACKGROUND/AIM: The treatment rate of Burkitt lymphoma (BL) is still low in low-income countries and among elderly patients. The c-Myc dysregulation induced by mutations is one of the characteristics of BL. However, studies on the downstream signaling pathways of c-Myc are still lacking. This study aimed to identify the signaling pathways regulated by c-Myc. MATERIALS AND METHODS: Network and gene set analyses using c-Myc inhibition (i.e., c-Myc knock-down and c-Myc inhibitor treatment) transcriptome datasets for BL cell lines were performed to determine the pathways regulated by c-Myc. In addition, computational drug repurposing was used to identify drugs that can regulate c-Myc downstream signaling pathway. RESULTS: Computational drug repurposing revealed that the ERK/MAPK signaling pathway is regulated by c-Myc in BL and that this pathway can be modulated by vorinostat. Furthermore, in the pharmacogenomics database, vorinostat showed a cell viability half-maximal inhibitory concentration of less than 2 μM in the BL cell lines. CONCLUSION: The downstream signaling pathway regulated by c-Myc and the drug that can modulate this pathway is presented for the first time. Copyright © 2023, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.
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