ReviewFrontiers in immunology2022
Purinergic receptors are a key bottleneck in tumor metabolic reprogramming: The prime suspect in cancer therapeutic resistance.
Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- ATP is not always pro-inflammatory: rethinking purinergic signalling in cancer and autoimmunity.Purinergic signalling · 2026Review
- The controversial role of metabolic reprogramming in anti-tumor therapy resistance.Discover oncology · 2026Review
- Defective biological networks associated with pseudogene-derived lncRNAs in cancer drug resistance: Promising prospects for their clinical targets in cancer therapy.Genes & diseases · 2026Review
- Integrating Transcriptomics and 3D Spheroid Models Reveals Microenvironment-Dependent Purinergic Modulation in Hepatocellular Carcinoma.Metabolites · 2026Article
- The purinergic signaling interfaces in breast cancer angiogenesis.Purinergic signalling · 2026Review
- Purinergic receptors in atherosclerosis: implications for pathophysiology and therapeutic strategies.Journal of physiology and biochemistry · 2025Review
- Ap4A in Cancer: A Multifaceted Regulator and Emerging Therapeutic Target.Molecules (Basel, Switzerland) · 2025Review
- Purines and purinergic receptors in primary tumors of the central nervous system.Purinergic signalling · 2025Article
- On the Quest for Biomarkers: A Comprehensive Analysis of Modified Nucleosides in Ovarian Cancer Cell Lines.Cells · 2025Article
- IRX5 Promoted SREBP1-Mediated de Novo Fatty Acid Synthesis via HMGN4 in Hepatocellular Carcinoma.Journal of cellular and molecular medicine · 2025Article
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- Diverse temporal and spatial mechanisms work, partially through Stanniocalcin-1, V-ATPase and senescence, to activate the extracellular ATP-mediated drug resistance in human cancer cells.Frontiers in oncology · 2024Article
- Editorial: Targeting nucleotide metabolism for enhancing antitumor immunity.Frontiers in immunology · 2024Article
- Purinergic P2X7R as a potential target for pancreatic cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- Therapeutic targeting of P2X4 receptor and mitochondrial metabolism in clear cell renal carcinoma models.Journal of experimental & clinical cancer research : CR · 2023Article
- Transcriptomic and metabolomic analysis of peri-tumoral hepatic tissue in hepatocellular carcinoma: unveiling the molecular landscape of immune checkpoint therapy resistance.Frontiers in pharmacology · 2023Article
- Tumor Microenvironment and Metabolism: Role of the Mitochondrial Melatonergic Pathway in Determining Intercellular Interactions in a New Dynamic Homeostasis.International journal of molecular sciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ATP and other nucleoside phosphates have specific receptors named purinergic receptors. Purinergic receptors and ectonucleotidases regulate various signaling pathways that play a role in physiological and pathological processes. Extracellular ATP in the tumor microenvironment (TME) has a higher level than in normal tissues and plays a role in cancer cell growth, survival, angiogenesis, metastasis, and drug resistance. In this review, we investigated the role of purinergic receptors in the development of resistance to therapy through changes in tumor cell metabolism. When a cell transforms to neoplasia, its metabolic processes change. The metabolic reprogramming modified metabolic feature of the TME, that can cause impeding immune surveillance and promote cancer growth. The purinergic receptors contribute to therapy resistance by modifying cancer cells' glucose, lipid, and amino acid metabolism. Limiting the energy supply of cancer cells is one approach to overcoming resistance. Glycolysis inhibitors which reduce intracellular ATP levels may make cancer cells more susceptible to anti-cancer therapies. The loss of the P2X7R through glucose intolerance and decreased fatty acid metabolism reduces therapeutic resistance. Potential metabolic blockers that can be employed in combination with other therapies will aid in the discovery of new anti-cancer immunotherapy to overcome therapy resistance. Therefore, therapeutic interventions that are considered to inhibit cancer cell metabolism and purinergic receptors simultaneously can potentially reduce resistance to treatment.
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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 Socratic graph.