ArticleScientific reports2025
TRIP13 alters mitochondrial function and promotes bortezomib resistance in multiple myeloma.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Integrative multi-omics profiling reveals an association between lipid metabolism dysregulation and bortezomib-induced cerebral hemorrhage in zebrafish.Fluids and barriers of the CNS · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors.
Funding
Abstract
Bortezomib (BTZ) resistance remains a major therapeutic challenge in multiple myeloma (MM). This study investigates the role of thyroid hormone receptor interactor 13 (TRIP13) in MM progression and BTZ resistance. Analysis of public datasets and clinical bone marrow samples revealed that TRIP13 is significantly upregulated in MM and that its expression correlates with advanced disease stage and poor overall survival. In vitro, TRIP13 overexpression (TRIP13-OE) in MM cell lines significantly enhanced cell proliferation, reduced BTZ-induced apoptosis, and alleviated G2/M cell cycle arrest. Functional assays further showed that TRIP13-OE cells preserved mitochondrial membrane potential, reduced mitochondrial calcium overload, and maintained ATP production following BTZ exposure. Quantitative polymerase chain reaction (qPCR) analysis demonstrated that mitochondrial regulatory genes were upregulated in TRIP13-OE cells, particularly mitochondrial calcium uniporter (MCU). Co-immunoprecipitation following BTZ treatment confirmed a specific interaction between TRIP13 and MCU, while immunofluorescence labeling showed their cytoplasmic co-localization. These findings uncover a previously unrecognized role of TRIP13 in regulating mitochondrial integrity under proteotoxic stress, thereby contributing to BTZ resistance. Targeting TRIP13 may represent a novel therapeutic approach to improve outcomes in MM patients.
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