ArticleInternational journal of molecular sciences2013
Acidosis decreases c-Myc oncogene expression in human lymphoma cells: a role for the proton-sensing G protein-coupled receptor TDAG8.
Article in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 47 citations in OpenAlex.
- Loss of proton-sensing TDAG8 increases tumor progression in mouse models of colon cancer.Molecular oncology · 2026Article
- Epigenomic and Metabolic Interplay in the Development of Metastatic Brain Tumors.Oncology research · 2026Review
- GPR65 Functions as a Key Factor of Bone Aging and a Novel Therapeutic Target for Osteoporosis.Aging cell · 2025Article
- Acidic Tumor Microenvironments and Emerging Therapeutic Strategies for Cancer Therapy.Yonsei medical journal · 2025Review
- Review
- Proton Sensing GPCR's: The missing link to Warburg's Oncogenic Legacy?Journal of cancer biology · 2024Article
- Lactate: a rising star in tumors and inflammation.Frontiers in immunology · 2024Review
- Targeting GPR65 alleviates hepatic inflammation and fibrosis by suppressing the JNK and NF-κB pathways.Military Medical Research · 2023Article
- Location-biased activation of the proton-sensor GPR65 is uncoupled from receptor trafficking.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- GPR65 inhibits human trophoblast cell adhesion through upregulation of MYLK and downregulation of fibronectin via cAMP-ERK signaling in a low pH environment.Cell communication and signaling : CCS · 2023Article
- GPR65 as a potential immune checkpoint regulates the immune microenvironment according to pan-cancer analysis.Heliyon · 2023Article
- Identification and Validation of Prognostic Biomarkers Specifically Expressed in Macrophage in IgA Nephropathy Patients Based on Integrated Bioinformatics Analyses.Frontiers in molecular biosciences · 2022Article
- GPR65 (TDAG8) inhibits intestinal inflammation and colitis-associated colorectal cancer development in experimental mouse models.Biochimica et biophysica acta. Molecular basis of disease · 2022Article
- Proton-Sensing GPCRs in Health and Disease.Cells · 2021Review
- Cancer cell metabolic reprogramming: a keystone for the response to immunotherapy.Cell death & disease · 2020Review
- Review
- Proton-sensing G protein-coupled receptors: detectors of tumor acidosis and candidate drug targets.Future medicinal chemistry · 2020Review
- Article
- Metabolic Barriers to T Cell Function in Tumors.Journal of immunology (Baltimore, Md. : 1950) · 2018Review
- Contextual tumor suppressor function of T cell death-associated gene 8 (TDAG8) in hematological malignancies.Journal of translational medicine · 2017Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acidosis is a biochemical hallmark of the tumor microenvironment. Here, we report that acute acidosis decreases c-Myc oncogene expression in U937 human lymphoma cells. The level of c-Myc transcripts, but not mRNA or protein stability, contributes to c-Myc protein reduction under acidosis. The pH-sensing receptor TDAG8 (GPR65) is involved in acidosis-induced c-Myc downregulation. TDAG8 is expressed in U937 lymphoma cells, and the overexpression or knockdown of TDAG8 further decreases or partially rescues c-Myc expression, respectively. Acidic pH alone is insufficient to reduce c-Myc expression, as it does not decrease c-Myc in H1299 lung cancer cells expressing very low levels of pH-sensing G protein-coupled receptors (GPCRs). Instead, c-Myc is slightly increased by acidosis in H1299 cells, but this increase is completely inhibited by ectopic overexpression of TDAG8. Interestingly, TDAG8 expression is decreased by more than 50% in human lymphoma samples in comparison to non-tumorous lymph nodes and spleens, suggesting a potential tumor suppressor function of TDAG8 in lymphoma. Collectively, our results identify a novel mechanism of c-Myc regulation by acidosis in the tumor microenvironment and indicate that modulation of TDAG8 and related pH-sensing receptor pathways may be exploited as a new approach to inhibit Myc expression.
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