ArticleAmerican journal of translational research2019
BTK induces CAM-DR through regulation of CXCR4 degradation in multiple myeloma.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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
5 citing papers in PubMed, 8 citations in OpenAlex.
- Pathways to therapy resistance: The sheltering effect of the bone marrow microenvironment to multiple myeloma cells.Heliyon · 2024Review
- Review
- Article
- Targeting RFWD2 as an Effective Strategy to Inhibit Cellular Proliferation and Overcome Drug Resistance to Proteasome Inhibitor in Multiple Myeloma.Frontiers in cell and developmental biology · 2021Article
- CAM-DR: Mechanisms, Roles and Clinical Application in Tumors.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular adhesion-mediated drug resistance (CAM-DR) occurs frequently in patients with relapsed or refractory multiple myeloma (MM). Elucidating the mechanism underlying CAM-DR and developing the corresponding treatment may prove to be promising for the clinical management of MM. Bruton's tyrosine kinase (BTK) has been attracting attention in relation to MM progression and drug resistance. BTK was reported to be associated with cell surface CXCR4, a classic cell adhesion molecule and homing factor. However, the exact association between BTK and CAM-DR in MM remains elusive. In this study, we demonstrated that promoting BTK expression induced MM cell adherence to the extracellular matrix (ECM) and stromal cells in vitro and in vivo, and that CAM-DR could be reversed by separating MM cells from ECM or stromal cells. Enhancing BTK expression levels increased CXCR4 expression in MM cells. In addition, BTK may bind directly with CXCR4 and prevent its ubiquitination-induced degradation. Finally, a BTK inhibitor exerted synergistic therapeutic effects with bortezomib in a 5TMM3VT MM mouse model. These findings revealed a novel role of BTK in CAM-DR and may provide a promising approach to MM treatment.
Indexed as
Identifiers
31396324PMC6684885W2984862478What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.