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Elevated PRKD2 Promotes Progression and Poor Prognosis of Multiple Myeloma

ABSTRACT: This study aimed to address the challenges in treating multiple myeloma (MM) and its advanced stage, relapsed and refractory multiple myeloma (RRMM), by identifying new therapeutic targets. Clinical data were collected from 132 MM patients. Through propensity score matching, bone marrow samples from 24 MM patients and 6 control individuals were selected for RNA sequencing analysis. Western blot validation was performed in cell lines to investigate the role of serine/threonine-protein kinase D2 (PRKD2) in MM and RRMM. Additionally, gene ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, immune infiltration analysis, and drug sensitivity screening were conducted. The study found PRKD2 to be significantly upregulated in MM and RRMM, suggesting its potential as a therapeutic target. Functional assays indicated that disrupting PRKD2 inhibited myeloma cell proliferation, and pathway analysis revealed immune-related pathway alterations associated with PRKD2 expression. Drug sensitivity analysis identified Axitinib as a potential therapeutic agent targeting PRKD2, highlighting its promise for MM treatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE268395 | GEO | 2025/09/09

REPOSITORIES: GEO

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Genome-wide analysis of gene expression in response to bortezomib treatment [human cell lines].

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2013-07-02 | E-GEOD-41927 | biostudies-arrayexpress

Genome-wide analysis of gene expression in response to bortezomib treatment [mouse cell lines I]

Project description:Genome-wide analysis of gene expression in response to bortezomib treatment (33 nM) in cell lines before and after selection for resistance. Multiple myeloma (MM) is a hematologic malignancy characterized by the proliferation of neoplastic plasma cells in the bone marrow. While the first-to-market proteasome inhibitor bortezomib/VELCADE has been successfully used to treat myeloma patients, drug resistance remains an emerging problem. In this study, we identify signatures of bortezomib sensitivity and resistance by gene expression profiling (GEP) using pairs of bortezomib-sensitive and -resistant cell lines created from the Bcl-XL/Myc double transgenic mouse model of MM. Finally, these data reveal complex heterogeneity within MM and suggest resistance to one drug class reprograms resistant clones to make them more sensitive to a distinct class of drugs. This study represents an important next step in translating pharmacogenomic profiling and may be useful for understanding personalized pharmacotherapy of MM patients.

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