ArticleThe Journal of biological chemistry2018
Hyaluronan and proteoglycan link protein 1 (HAPLN1) activates bortezomib-resistant NF-κB activity and increases drug resistance in multiple myeloma.
Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 42 citations in OpenAlex.
- Extracellular matrix dynamics in tumor immunoregulation: from tumor microenvironment to immunotherapy.Journal of hematology & oncology · 2025Review
- Proteasome: Role in T Cell Function Regulation.International journal of biological sciences · 2025Review
- miR‑1343‑3p inhibits autophagy by directly targeting ATG7 in multiple myeloma cells.Biomedical reports · 2024Article
- Dynamic Organization of Neuronal Extracellular Matrix Revealed by HaloTag-HAPLN1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Novel extracellular matrix architecture on excitatory neurons revealed by HaloTag-HAPLN1.bioRxiv : the preprint server for biology · 2024Article
- Multidimensional role of adapalene in regulating cell death in multiple myeloma.Frontiers in pharmacology · 2024Article
- HAPLN1 matrikine: a bone marrow homing factor linked to poor outcomes in patients with MM.Blood advances · 2023Article
- Hyaluronan and Proteoglycan Link Protein 1 Activates the BMP4/Smad1/5/8 Signaling Pathway to Promote Osteogenic Differentiation: an Implication in Fracture Healing.Molecular biotechnology · 2023Article
- HAPLN1 potentiates peritoneal metastasis in pancreatic cancer.Nature communications · 2023Article
- Ectopic CH60 mediates HAPLN1-induced cell survival signaling in multiple myeloma.Life science alliance · 2023Article
- A novel glycolysis-related gene signature for predicting the prognosis of multiple myeloma.Frontiers in cell and developmental biology · 2023Article
- A Hyaluronan and Proteoglycan Link Protein 1 Matrikine: Role of Matrix Metalloproteinase 2 in Multiple Myeloma NF-κB Activation and Drug Resistance.Molecular cancer research : MCR · 2022Article
- Matrix proteoglycans in tumor inflammation and immunity.American journal of physiology. Cell physiology · 2022Review
- Posttranslational modification of Aurora A-NSD2 loop contributes to drug resistance in t(4;14) multiple myeloma.Clinical and translational medicine · 2022Article
- Cancer-associated fibroblasts-derived HAPLN1 promotes tumour invasion through extracellular matrix remodeling in gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2022Article
- HAPLN1 Affects Cell Viability and Promotes the Pro-Inflammatory Phenotype of Fibroblast-Like Synoviocytes.Frontiers in immunology · 2022Article
- HAPLN1 confers multiple myeloma cell resistance to several classes of therapeutic drugs.PloS one · 2022Article
- Article
- Treatment Advances in EBV Related Lymphoproliferative Diseases.Frontiers in oncology · 2022Review
- Research progress in proteasome inhibitor resistance to multiple myeloma.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2021Article
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
Nuclear factor-κB (NF-κB) is a family of transcription factors that play a key role in cell survival and proliferation in many hematological malignancies, including multiple myeloma (MM). Bortezomib, a proteasome inhibitor used in the management of MM, can inhibit both canonical and noncanonical activation of NF-κB in MM cells. However, we previously reported that a significant fraction of freshly isolated MM cells harbor bortezomib-resistant NF-κB activity. Here, we report that hyaluronan and proteoglycan link protein 1 (HAPLN1) is produced in bone marrow stromal cells from MM patients, is detected in patients' bone marrow plasma, and can activate an atypical bortezomib-resistant NF-κB pathway in MM cells. We found that this pathway involves bortezomib-resistant degradation of the inhibitor of NF-κB (IκBα), despite efficient bortezomib-mediated inhibition of proteasome activity. Moreover, HAPLN1 can also confer bortezomib-resistant survival of MM cells. We propose that HAPLN1 is a novel pathogenic factor in MM that induces an atypical NF-κB activation and thereby promotes bortezomib resistance in MM cells.
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