ArticleScientific reports2016
Dies1/VISTA expression loss is a recurrent event in gastric cancer due to epigenetic regulation.
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 24 papers.
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The trial behind it
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Who cites it
24 citing papers in PubMed, 34 citations in OpenAlex.
- VISTA drives tumour-intrinsic proliferation in mesothelioma cells.British journal of cancer · 2026Article
- VISTA: An Emerging Immune Checkpoint With Clinical Relevance Across Diverse Malignancies.Immune network · 2025Review
- The B7 family molecules in oral squamous cell carcinoma: a systematic review. Part II: B7-1, B7-2, B7-H2, B7-H3, B7-H4, B7-H5 (VISTA), B7-H6 and B7-H7.Postepy dermatologii i alergologii · 2025Review
- Pan-cancer analysis of co-inhibitory molecules revealing their potential prognostic and clinical values in immunotherapy.Frontiers in immunology · 2025Article
- VISTA-mediated immune evasion in cancer.Experimental & molecular medicine · 2024Review
- VISTA and its ligands: the next generation of promising therapeutic targets in immunotherapy.Cancer cell international · 2023Review
- VISTA as a prospective immune checkpoint in gynecological malignant tumors: A review of the literature.Open medicine (Warsaw, Poland) · 2023Review
- The expression of VISTA on CD4+ T cells associate with poor prognosis and immune status in non-small cell lung cancer patients.Bosnian journal of basic medical sciences · 2022Article
- Article
- The Features of Checkpoint Receptor-Ligand Interaction in Cancer and the Therapeutic Effectiveness of Their Inhibition.Biomedicines · 2022Review
- The Features of Immune Checkpoint Gene Regulation by microRNA in Cancer.International journal of molecular sciences · 2022Review
- IGSF11 and VISTA: a pair of promising immune checkpoints in tumor immunotherapy.Biomarker research · 2022Review
- miR-125a-5p promotes gastric cancer growth and invasion by regulating the Hippo pathway.Journal of clinical laboratory analysis · 2021Article
- The Positive and Negative Immunoregulatory Role of B7 Family: Promising Novel Targets in Gastric Cancer Treatment.International journal of molecular sciences · 2021Review
- Phytochemicals in Cancer Immune Checkpoint Inhibitor Therapy.Biomolecules · 2021Review
- The Regulatory Cross-Talk between microRNAs and Novel Members of the B7 Family in Human Diseases: A Scoping Review.International journal of molecular sciences · 2021Article
- VISTA Blockade Aggravates Bone Loss in Experimental Murine Apical Periodontitis.Frontiers in immunology · 2021Article
- The Role of V-Domain Ig Suppressor of T Cell Activation (VISTA) in Cancer Therapy: Lessons Learned and the Road Ahead.Frontiers in immunology · 2021Review
- Immune Checkpoints, a Novel Class of Therapeutic Targets for Autoimmune Diseases.Frontiers in immunology · 2021Review
- VISTA: a novel immunotherapy target for normalizing innate and adaptive immunity.Seminars in immunology · 2019Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dies1/VISTA induces embryonic stem-cell differentiation, via BMP-pathway, but also acts as inflammation regulator and immune-response modulator. Dies1 inhibition in a melanoma-mouse model led to increased tumour-infiltrating T-cells and decreased tumour growth, emphasizing Dies1 relevance in tumour-microenvironment. Dies1 is involved in cell de/differentiation, inflammation and cancer processes, which mimic those associated with Epithelial-to-Mesenchymal-Transition (EMT). Despite this axis linking Dies1 with EMT and cancer, its expression, modulation and relevance in these contexts is unknown. To address this, we analysed Dies1 expression, its regulation by promoter-methylation and miR-125a-5p overexpression, and its association with BMP-pathway downstream-effectors, in a TGFβ1-induced EMT-model, cancer cell-lines and primary samples. We detected promoter-methylation as a mechanism controlling Dies1 expression in our EMT-model and in several cancer cell-lines. We showed that the relationship between Dies1 expression and BMP-pathway effectors observed in the EMT-model, was not present in all cell-lines, suggesting that Dies1 has other cell-specific effectors, beyond the BMP-pathway. We further demonstrated that: Dies1 expression loss is a recurrent event in GC, caused by promoter methylation and/or miR-125a-5p overexpression and; GC-microenvironment myofibroblasts overexpress Dies1. Our findings highlight Dies1 as a novel player in GC, with distinct roles within tumour cells and in the tumour-microenvironment.
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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.