Evidence map›Paper›PMID 39430832›Full record

ArticleTranslational cancer research2024

Bioinformatics study of bortezomib resistance-related proteins and signaling pathways in mantle cell lymphoma.

Linyi Zheng, Qian Shen, Guanghong Fang, Ian J Robertson, Qiqiang Long

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Article in Translational cancer research, 2024. 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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5 · Who and what money

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5 authors.

Linyi ZhengDepartment of Hematology, The Second Hospital of Nanjing, Nanjing University of Chinese Medicine, Nanjing, China.
Qian ShenDepartment of Hematologic Lymphoma, Affiliated Tumor Hospital of Nantong University, Nantong, China.
Guanghong FangDepartment of Rehabilitation Medicine, Minghe Rehabilitation Hospital, Shuyang, China.
Ian J RobertsonDepartment of Internal Medicine, Walter Reed National Military Medical Center, Bethesda, MD, USA.
Qiqiang LongDepartment of Hematology, The Second Hospital of Nanjing, Nanjing University of Chinese Medicine, Nanjing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The bortezomib (BTZ) resistance mechanisms in mantle cell lymphoma (MCL) are complex, involving various genes and signaling pathways. This study used bioinformatical tools to identify and analyze differentially expressed genes (DEGs) associated with BTZ resistance. Methods: Gene chip datasets containing MCL BTZ-resistant and normal control cohorts (GSE20915 and GSE51371) were selected from the Gene Expression Omnibus (GEO) database. GEO2R was used to identify the upregulated DEGs in the microarray datasets, using a significance threshold of P<0.05. Subsequently, these DEGs were subjected to a Gene Ontology (GO) functional analysis, a Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and a protein-protein interaction (PPI) network assessment. Additionally, 40 MCL patients who underwent second-line BTZ treatment were included in this study. The patients were categorized into resistant and sensitive groups based on treatment response. The enzyme-linked immunosorbent assay (ELISA) technique was employed to evaluate the expression levels of specific DEGs in the serum of the patients in both groups. Results: In the GSE20915 dataset, 144 upregulated genes were identified as DEGs. Similarly, in the GSE51371 dataset, 219 upregulated genes were identified as DEGs. By employing a Venn diagram to compare the upregulated DEGs from both datasets, we identified 11 DEGs linked to BTZ resistance in MCL. The enrichment analysis of the KEGG signaling pathways revealed that the DEGs were predominantly enriched in key biological processes (BP), including the cell cycle, cellular senescence, the p53 signaling pathway, the interleukin 17 (IL-17) signaling pathway, and the nuclear factor kappa-B (NF-κB) signaling pathway. A distinct cluster was revealed by creating a PPI network and performing a module analysis of a set of typical DEGs. This cluster comprised four candidate genes; that is, cyclin-dependent kinase inhibitor 1A ( Conclusion: Identifying the key gene

Indexed as

bioinformaticsbortezomib (BTZ)Mantle cell lymphoma (MCL)resistancetarget genes

Identifiers

PMID39430832
PMCPMC11483405

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