ArticleCancer research2014
The niacin/butyrate receptor GPR109A suppresses mammary tumorigenesis by inhibiting cell survival.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 130 citations in OpenAlex.
- Shaping death: how the microbiome regulates tumour cell demise and therapy response.Cancer metastasis reviews · 2026Review
- Gut microbiome-driven colorectal cancer via immune, metabolic, neural, and endocrine axes reprogramming.NPJ biofilms and microbiomes · 2026Review
- Niacin, an active form of vitamin B3, exerts antiviral function by recruiting β-arrestin through GPR109A to activate the phosphorylation of ERK and STAT1 axis.Journal of virology · 2025Article
- Sex dependent effects of GPR109A gene deletion in myeloid cells on bone development in mice.Scientific reports · 2025Article
- Structures of G-protein coupled receptor HCAR1 in complex with Gi1 protein reveal the mechanistic basis for ligand recognition and agonist selectivity.PLoS biology · 2025Article
- Gut microbiome and lung cancer: mechanisms, interactions, and dietary interventions.Gut microbes reports · 2025Review
- Microbiota-derived metabolites in tumorigenesis: mechanistic insights and therapeutic implications.Frontiers in pharmacology · 2025Review
- The survival of B cells is compromised in kidney disease.Nature communications · 2024Article
- Targeting ketone body metabolism in mitigating gemcitabine resistance.JCI insight · 2024Article
- Influence of the gut microbiota on immune cell interactions and cancer treatment.Journal of translational medicine · 2024Review
- Taking SCFAs produced by Lactobacillus reuteri orally reshapes gut microbiota and elicits antitumor responses.Journal of nanobiotechnology · 2024Article
- Lipid-lowering drugs and cancer: an updated perspective.Pharmacological reports : PR · 2024Review
- The role of short-chain fatty acid metabolism in the pathogenesis, diagnosis and treatment of cancer.Frontiers in oncology · 2024Review
- CD72, a new immune checkpoint molecule, is a novel prognostic biomarker for kidney renal clear cell carcinoma.European journal of medical research · 2023Article
- Ebola Virus Infection Induces HCAR2 Expression Leading to Cell Death.The Journal of infectious diseases · 2023Article
- Signaling pathways in cancer metabolism: mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Emerging roles of GPR109A in regulation of neuroinflammation in neurological diseases and pain.Neural regeneration research · 2023Review
- Control of Redox Homeostasis by Short-Chain Fatty Acids: Implications for the Prevention and Treatment of Breast Cancer.Pathogens (Basel, Switzerland) · 2023Review
- Molecular Mechanisms for Ketone Body Metabolism, Signaling Functions, and Therapeutic Potential in Cancer.Nutrients · 2022Review
- The Function and Molecular Mechanism of Commensal Microbiome in Promoting Malignant Progression of Lung Cancer.Cancers · 2022Review
5 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
GPR109A, a G-protein-coupled receptor, is activated by niacin and butyrate. Upon activation in colonocytes, GPR109A potentiates anti-inflammatory pathways, induces apoptosis, and protects against inflammation-induced colon cancer. In contrast, GPR109A activation in keratinocytes induces flushing by activation of Cox-2-dependent inflammatory signaling, and the receptor expression is upregulated in human epidermoid carcinoma. Thus, depending on the cellular context and tissue, GPR109A functions either as a tumor suppressor or a tumor promoter. However, the expression status and the functional implications of this receptor in the mammary epithelium are not known. Here, we show that GPR109A is expressed in normal mammary tissue and, irrespective of the hormone receptor status, its expression is silenced in human primary breast tumor tissues, breast cancer cell lines, and in tumor tissues of three different murine mammary tumor models. Functional expression of this receptor in human breast cancer cell lines decreases cyclic AMP production, induces apoptosis, and blocks colony formation and mammary tumor growth. Transcriptome analysis revealed that GPR109A activation inhibits genes, which are involved in cell survival and antiapoptotic signaling, in human breast cancer cells. In addition, deletion of Gpr109a in mice increased tumor incidence and triggered early onset of mammary tumorigenesis with increased lung metastasis in MMTV-Neu mouse model of spontaneous breast cancer. These findings suggest that GPR109A is a tumor suppressor in mammary gland and that pharmacologic induction of this gene in tumor tissues followed by its activation with agonists could be an effective therapeutic strategy to treat breast cancer.
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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.