ArticleBlood advances2021
The fatty acid elongase ELOVL6 regulates bortezomib resistance in multiple myeloma.
Article in Blood advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Gene expression-based dissemination score predicts early spread and poor outcomes in multiple myeloma.Leukemia · 2026Article
- Targeting STK17B kinase activates ferroptosis and suppresses drug resistance in multiple myeloma.Blood · 2026Article
- Prognostic value of fatty acid metabolism-related signature and integrated analysis of the immune microenvironment in multiple myeloma.BMC cancer · 2025Article
- Carfilzomib resistance in multiple myeloma: A comparative metabolomic analysis.Journal of applied genetics · 2025Article
- Acid ceramidase controls proteasome inhibitor resistance and is a novel therapeutic target for the treatment of relapsed/refractory multiple myeloma.Haematologica · 2025Article
- Article
- Acquired Bortezomib Resistance in Multiple Myeloma: From Mechanisms to Strategy.Current treatment options in oncology · 2024Review
- Acute suppression of translation by hyperthermia enhances anti-myeloma activity of carfilzomib.International journal of hematology · 2024Article
- Lipid metabolic vulnerabilities of multiple myeloma.Clinical and experimental medicine · 2023Review
- Metabolic Alterations in Multiple Myeloma: From Oncogenesis to Proteasome Inhibitor Resistance.Cancers · 2023Review
- Article
- Obesity and myeloma: Clinical and mechanistic contributions to disease progression.Frontiers in endocrinology · 2023Review
- Article
- Emerging Roles of Lipophagy in Cancer Metastasis.Cancers · 2022Review
- Reprogramming lipid metabolism as potential strategy for hematological malignancy therapy.Frontiers in oncology · 2022Review
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Resistance to the proteasome inhibitor bortezomib (BTZ) represents a major obstacle in the treatment of multiple myeloma (MM). The contribution of lipid metabolism in the resistance of MM cells to BTZ is mostly unknown. Here we report that levels of fatty acid elongase 6 (ELOVL6) were lower in MM cells from BTZ-nonresponsive vs BTZ-responsive patients and in cultured MM cells selected for BTZ resistance compared with parental counterparts. Accordingly, depletion of ELOVL6 in parental MM cells suppressed BTZ-induced endoplasmic reticulum (ER) stress and cytotoxicity, whereas restoration of ELOVL6 levels in BTZ-resistant MM cells sensitized them to BTZ in tissue culture settings and, as xenografts, in a plasmacytoma mouse model. Furthermore, for the first time, we identified changes in the BTZ-induced lipidome between parental and BTZ-resistant MM cell lines underlying a functional difference in their response to BTZ. We demonstrated that restoration of ELOVL6 levels in BTZ-resistant MM cells resensitized them to BTZ largely via upregulation of ELOVL6-dependent ceramide species, which was a prerequisite for BTZ-induced ER stress and cell death in these cells. Our data characterize ELOVL6 as a major clinically relevant regulator of MM cell resistance to BTZ, which can emerge from the impaired ability of these cells to alter ceramide composition in response to BTZ.
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