ArticleScientific reports2016
The accessory proteins REEP5 and REEP6 refine CXCR1-mediated cellular responses and lung cancer progression.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- EMT activates ER-to-Golgi trafficking through upregulation of REEP2 to promote lung cancer progression.Research square · 2026Article
- The expression significance and non-invasive detection of REEP6 and REEP5 in prostate cancer.BMC cancer · 2026Article
- Subcellular Proteomic Analyses Reveal REEP5 Knockdown in the Mouse Heart Disrupts Mitochondrial Networks.Molecular & cellular proteomics : MCP · 2026Article
- REEP6 promotes colorectal cancer glycolysis and tumorigenesis through PRMT5-mediated PGAM1 arginine methylation.Acta pharmaceutica Sinica. B · 2026Article
- Lung scRNA-seq reveals chronic inflammation and emphysemous phenotype in mice with osteogenesis imperfecta.Frontiers in genetics · 2026Article
- EMT activates ER-to-Golgi trafficking through upregulation of REEP2 to promote lung cancer progression.bioRxiv : the preprint server for biology · 2025Article
- Serum fucosylated receptor expression-enhancing protein 5 as a biomarker for early stage pancreatic cancer.Oncology letters · 2025Article
- A preliminary investigation of the differences in immune responses in different strains of mice with localized allergic rhinitis tolerance models.The World Allergy Organization journal · 2025Article
- LncRNA-MALAT1 promotes triple-negative breast cancer progression and function as ceRNA to target REEP5 by sponging miR-106a-5p.European journal of medical research · 2025Article
- REEP4 as Potential Biomarker Associated with Predictive Prognosis and Immune Response in Kidney Clear Cell Carcinoma.Journal of Cancer · 2024Article
- From Cell to Symptoms: The Role of SARS-CoV-2 Cytopathic Effects in the Pathogenesis of COVID-19 and Long COVID.International journal of molecular sciences · 2023Review
- The Clinical and Biological Effects of Receptor Expression-Enhancing Protein 6 in Tongue Squamous Cell Carcinoma.Biomedicines · 2023Article
- Applicability of Anticancer Drugs for the Triple-Negative Breast Cancer Based on Homologous Recombination Repair Deficiency.Frontiers in cell and developmental biology · 2022Article
- Enzymes in the Cholesterol Synthesis Pathway: Interactomics in the Cancer Context.Biomedicines · 2021Article
- Circular RNA hsa_circ_0000700 promotes cell proliferation and migration in Esophageal Squamous Cell Carcinoma by sponging miR-1229.Journal of Cancer · 2021Article
- Proteome-wide data analysis reveals tissue-specific network associated with SARS-CoV-2 infection.Journal of molecular cell biology · 2020Article
- Pregnancy reprograms the epigenome of mammary epithelial cells and blocks the development of premalignant lesions.Nature communications · 2020Article
- Knockout of mouse receptor accessory protein 6 leads to sperm function and morphology defects†.Biology of reproduction · 2020Article
- Identification of Important Modules and Biomarkers in Breast Cancer Based on WGCNA.OncoTargets and therapy · 2020Article
- Gene Therapy Rescues Retinal Degeneration in Receptor Expression-Enhancing Protein 6 Mutant Mice.Human gene therapy · 2019Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Some G-protein-coupled receptors have been reported to require accessory proteins with specificity for proper functional expression. In this study, we found that CXCR1 interacted with REEP5 and REEP6, but CXCR2 did not. Overexpression of REEP5 and REEP6 enhanced IL-8-stimulated cellular responses through CXCR1, whereas depletion of the proteins led to the downregulation of the responses. Although REEPs enhanced the expression of a subset of GPCRs, in the absence of REEP5 and REEP6, CXCR1 was expressed in the plasma membrane, but receptor internalization and intracellular clustering of β-arrestin2 following IL-8 treatment were impaired, suggesting that REEP5 and REEP6 might be involved in the ligand-stimulated endocytosis of CXCR1 rather than membrane expression, which resulted in strong cellular responses. In A549 lung cancer cells, which endogenously express CXCR1, the depletion of REEP5 and REEP6 significantly reduced growth and invasion by downregulating IL-8-stimulated ERK phosphorylation, actin polymerization and the expression of genes related to metastasis. Furthermore, an in vivo xenograft model showed that proliferation and metastasis of A549 cells lacking REEP5 and REEP6 were markedly decreased compared to the control group. Thus, REEP5 and REEP6 could be novel regulators of G-protein-coupled receptor signaling whose functional mechanisms differ from other accessory proteins.
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