ArticleThe Journal of clinical investigation2024
LOXL2-induced PEAR1 Ser891 phosphorylation suppresses CD44 degradation and promotes triple-negative breast cancer metastasis.
Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Comparison of variably specific Bruton tyrosine kinase inhibitors on platelet aggregation mediated by Fcγ receptor (FcγR) IIa, glycoprotein VI, and platelet endothelial aggregation receptor (PEAR) 1: implications for Bruton tyrosine kinase inhibitors as antithrombotic therapy.Research and practice in thrombosis and haemostasis · 2026Article
- Ultrasound-targeted microbubble cavitation enhances anti-PD-L1 therapy in TNBC via eNOS-mediated reoxygenation.JCI insight · 2026Article
- CDK2-Mediated Phosphorylation ofResearch (Washington, D.C.) · 2026Article
- Lung endothelial PEAR1 induces tumor cell dormancy.Molecular cancer · 2025Article
- Targeting MTAP increases PARP inhibitor susceptibility in triple-negative breast cancer through a feed-forward loop.The Journal of clinical investigation · 2025Article
- Noncoding RNA-encoded peptides in cancer: biological functions, posttranslational modifications and therapeutic potential.Journal of hematology & oncology · 2025Review
- A Multi-Faceted Approach to Explore the Role of Inflammatory CAFs, Providing Prognostic Value and Therapeutic Implications in Lung Adenocarcinoma.International journal of genomics · 2025Article
- Inhibition of LOXL2 Suppresses Nasal Mucosal Inflammation and Remodeling in Allergic Rhinitis.Journal of asthma and allergy · 2025Article
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD44 is associated with a high risk of metastasis, recurrence, and drug resistance in various cancers. Here we report that platelet endothelial aggregation receptor 1 (PEAR1) is a CD44 chaperone protein that protected CD44 from endocytosis-mediated degradation and enhances cleavage of the CD44 intracellular domain (CD44-ICD). Furthermore, we found that lysyl oxidase-like protein 2 (LOXL2), an endogenous ligand of PEAR1, bound to the PEAR1-EMI domain and facilitated the interaction between PEAR1 and CD44 by inducing PEAR1 Ser891 phosphorylation in a manner that was independent of its enzyme activity. Levels of PEAR1 protein and PEAR1 phosphorylation at Ser891 were increased in patients with triple-negative breast cancer (TNBC), were positively correlated with expression of LOXL2 and CD44, and were negatively correlated with overall survival. The level of PEAR1 Ser891 phosphorylation was identified as the best independent prognostic factor in TNBC patients. The prognostic efficacy of the combination of PEAR1 phosphorylation at Ser891 and CD44 expression was superior to that of PEAR1 phosphorylation at Ser891 alone. Blocking the interaction between LOXL2 and PEAR1 with monoclonal antibodies significantly inhibited TNBC metastasis, representing a promising therapeutic strategy for TNBC.
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