ArticleAmerican journal of physiology. Cell physiology2016
ATP promotes cell survival via regulation of cytosolic [Ca2+] and Bcl-2/Bax ratio in lung cancer cells.
Article in American journal of physiology. Cell physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 83 citations in OpenAlex.
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- P2 purinergic receptors regulate the progression of colorectal cancer.Purinergic signalling · 2025Review
- Store-operated CaAmerican journal of physiology. Lung cellular and molecular physiology · 2025Article
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- Novel Camptothecin Derivative 9c with Enhanced Antitumor Activity via NSA2-EGFR-P53 Signaling Pathway.International journal of molecular sciences · 2025Article
- Role and Therapeutic Potential of P2X7 Receptor in Lung Cancer Progression.Current medicinal chemistry · 2025Review
- Molecular mechanisms of extracellular-ATP-mediated colorectal cancer progression: Implication of purinergic receptors-mediated nucleocytoplasmic shuttling of HuR.Purinergic signalling · 2024Article
- Adenosine triphosphate induced cell death: Mechanisms and implications in cancer biology and therapy.World journal of clinical oncology · 2023Review
- Lipid polymer hybrid nanoparticles: a custom-tailored next-generation approach for cancer therapeutics.Molecular cancer · 2023Review
- SARS-CoV-2 spike protein receptor-binding domain perturbates intracellular calcium homeostasis and impairs pulmonary vascular endothelial cells.Signal transduction and targeted therapy · 2023Article
- ATP purinergic receptor signalling promotes Sca-1Cell communication and signaling : CCS · 2023Article
- Pathophysiology and pathogenic mechanisms of pulmonary hypertension: role of membrane receptors, ion channels, and CaPhysiological reviews · 2023Review
- Research Progress in the Relationship Between P2X7R and Cervical Cancer.Reproductive sciences (Thousand Oaks, Calif.) · 2023Review
- Study on the Mechanism of Hydrolyzed Seawater Pearl Tablet in Treating Chronic Sleep Deprivation Mice Model.Endocrine, metabolic & immune disorders drug targets · 2023Article
- Mitochondria-specific peptide amphiphiles induce mitochondrial dysfunction and peripheral T-cell lymphomas (PTCL) damage.Annals of translational medicine · 2022Article
- The Purinergic Landscape of Non-Small Cell Lung Cancer.Cancers · 2022Review
- Toward a Treatment of Cancer: Design and In Vitro/In Vivo Evaluation of Uncharged Pyrazoline Derivatives as a Series of Novel SHP2 Inhibitors.International journal of molecular sciences · 2022Article
- Naturally occurring deamidated triosephosphate isomerase is a promising target for cell-selective therapy in cancer.Scientific reports · 2022Article
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Authors and funding
11 authors at 2 institutions in 1 country.
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Abstract
Adenosine triphosphate (ATP) is a ubiquitous extracellular messenger elevated in the tumor microenvironment. ATP regulates cell functions by acting on purinergic receptors (P2X and P2Y) and activating a series of intracellular signaling pathways. We examined ATP-induced Ca(2+) signaling and its effects on antiapoptotic (Bcl-2) and proapoptotic (Bax) proteins in normal human airway epithelial cells and lung cancer cells. Lung cancer cells exhibited two phases (transient and plateau phases) of increase in cytosolic [Ca(2+)] ([Ca(2+)]cyt) caused by ATP, while only the transient phase was observed in normal cells. Removal of extracellular Ca(2+) eliminated the plateau phase increase of [Ca(2+)]cyt in lung cancer cells, indicating that the plateau phase of [Ca(2+)]cyt increase is due to Ca(2+) influx. The distribution of P2X (P2X1-7) and P2Y (P2Y1, P2Y2, P2Y4, P2Y6, P2Y11) receptors was different between lung cancer cells and normal cells. Proapoptotic P2X7 was nearly undetectable in lung cancer cells, which may explain why lung cancer cells showed decreased cytotoxicity when treated with high concentration of ATP. The Bcl-2/Bax ratio was increased in lung cancer cells following treatment with ATP; however, the antiapoptotic protein Bcl-2 demonstrated more sensitivity to ATP than proapoptotic protein Bax. Decreasing extracellular Ca(2+) or chelating intracellular Ca(2+) with BAPTA-AM significantly inhibited ATP-induced increase in Bcl-2/Bax ratio, indicating that a rise in [Ca(2+)]cyt through Ca(2+) influx is the critical mediator for ATP-mediated increase in Bcl-2/Bax ratio. Therefore, despite high ATP levels in the tumor microenvironment, which would induce cell apoptosis in normal cells, the decreased P2X7 and elevated Bcl-2/Bax ratio in lung cancer cells may enable tumor cells to survive. Increasing the Bcl-2/Bax ratio by exposure to high extracellular ATP may, therefore, be an important selective pressure promoting transformation and cancer progression.
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