ArticleOncogenesis2018
Extracellular vesicle-mediated EBAG9 transfer from cancer cells to tumor microenvironment promotes immune escape and tumor progression.
Article in Oncogenesis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
- Obesity-driven extracellular vesicle signaling in cancer: mechanistic insights and clinical implications.Oncogenesis · 2026Review
- TM9SF1 drives the lipophagic flux via AMPK-ULK1 signaling to sustain metabolic fitness in HER2-positive breast cancer.Cell death & disease · 2025Article
- Natural and Bioengineered Extracellular Vesicles in Diagnosis, Monitoring and Treatment of Cancer.ACS nano · 2025Review
- Cancer cell-derived extracellular vesicles: a potential target for overcoming tumor immunotherapy resistance and immune evasion strategies.Frontiers in immunology · 2025Review
- The theragnostic advances of exosomes in managing leukaemia.Journal of cellular and molecular medicine · 2024Review
- Applications of Urinary Extracellular Vesicles in the Diagnosis and Active Surveillance of Prostate Cancer.Cancers · 2024Review
- Understanding the role of transmembrane 9 superfamily member 1 in bladder cancer pathogenesis.World journal of clinical oncology · 2024Article
- TM9SF1 promotes bladder cancer cell growth and infiltration.World journal of clinical oncology · 2024Article
- TM9SF1 is implicated in promoting the proliferation and invasion of bladder cancer cells.World journal of clinical oncology · 2024Article
- EBAG9-deficient mice display decreased bone mineral density with suppressed autophagy.iScience · 2024Article
- Identification of somatic mutation-driven enhancers and their clinical utility in breast cancer.iScience · 2024Article
- Tumor-derived exosomal PD-L1: a new perspective in PD-1/PD-L1 therapy for lung cancer.Frontiers in immunology · 2024Review
- Prostate cancer-derived small extracellular vesicle proteins: the hope in diagnosis, prognosis, and therapeutics.Journal of nanobiotechnology · 2023Review
- Exosomes carrying immune checkpoints, a promising therapeutic approach in cancer treatment.Medical oncology (Northwood, London, England) · 2022Review
- Targeted inhibition of tumor-derived exosomes as a novel therapeutic option for cancer.Experimental & molecular medicine · 2022Review
- Microfluidics for detection of exosomes and microRNAs in cancer: State of the art.Molecular therapy. Nucleic acids · 2022Review
- mCell discovery · 2022Article
- Tumor-Derived Exosomes in Tumor-Induced Immune Suppression.International journal of molecular sciences · 2022Review
- NEUROD1 predicts better prognosis in pancreatic cancer revealed by a TILs-based prognostic signature.Frontiers in pharmacology · 2022Article
- A Prognostic Model Based on mRNA Expression Analysis of Esophageal Squamous Cell Carcinoma.Frontiers in bioengineering and biotechnology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The antitumor immune response is a critical defense system that eliminates malignant cells. The failure of the system results in immune escape and proceeds to tumor growth. We have previously showed that estrogen receptor-binding fragment-associated antigen 9 (EBAG9) is a relevant cancer biomarker and facilities immune escape of cancers from the immune surveillance. EBAG9 in cancer cells suppresses T-cell infiltration into tumor in vivo, whereas that in host immune cells functions as a limiter for T-cell cytotoxicity. Considering that EBAG9 plays immune suppressive roles in both tumor and microenvironment, we here questioned whether EBAG9 is a transferable protein from cancer to surrounding T cells and affects antitumor immune response. In this study, we showed that spontaneous development of prostate cancer was repressed in a model of Ebag9 knockout mice crossed with transgenic adenocarcinoma of the mouse prostate (TRAMP) mice. We identified TM9SF1 as a collaborative EBAG9 interactor, which regulates epithelial-mesenchymal transition (EMT) in cancer cells. Notably, extracellular vesicles (EVs) from EBAG9-overexpressing prostate cancer cells have a potential to facilitate immune escape of tumors by inhibiting T-cell cytotoxicity and modulating immune-related gene expression in T cells. Furthermore, we showed that a neutralizing antibody for EBAG9 could rescue the EV-mediated immune suppression by recovering T-cell cytotoxicity. In addition to its autocrine functions in cancer cells, EBAG9 could behave as a new class of immune checkpoint that suppresses tumor immunity in a secretory manner. We propose that EBAG9-targeting cancer treatment could be alternative therapeutic options for advanced diseases, particularly for those with EBAG9 overexpression.
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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.