{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhan S"],"funding":["NIDCR NIH HHS","NCATS NIH HHS","NCI NIH HHS"],"pagination":["14032-14042"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12464967"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["25(38)"],"pubmed_abstract":["This study investigates sodium chloride nanoparticles (SCNPs) as radiosensitizers. In contrast to conventional radiosensitizers that rely on high-Z effects or DNA-targeted mechanisms, SCNPs potentiate radiation-induced cellular damage by perturbing ion homeostasis. Importantly, SCNPs by elevating intracellular sodium levels reverse the sodium/calcium exchanger (NCX), leading to calcium influx. This calcium surge not only amplifies radiation-induced cancer cell death but also activates the cGAS-STING pathway, leading to the production of type I interferons. In syngeneic head and neck cancer models, SCNPs significantly improve tumor control and long-term survival in combination with radiation, without inducing detectable toxicity. Mechanistic studies reveal that these therapeutic benefits ar"],"journal":["Nano letters"],"pubmed_title":["Sodium Chloride Nanoparticles Potentiate Radiation Therapy by Disrupting Osmolarity Balance and Enhancing Antitumor Immunity."],"pmcid":["PMC12464967"],"funding_grant_id":["R01 DE033433","R01 CA247769","R01 DE028351","R01 CA257851","UL1 TR002378","P30 CA138292","R01 DE033691"],"pubmed_authors":["Lai X","Yang W","Zheng Y","Li J","Yao Y","Feng Z","Zhan S","Xie J","Patel SB","Teng Y"],"additional_accession":[]},"is_claimable":false,"name":"Sodium Chloride Nanoparticles Potentiate Radiation Therapy by Disrupting Osmolarity Balance and Enhancing Antitumor Immunity.","description":"This study investigates sodium chloride nanoparticles (SCNPs) as radiosensitizers. In contrast to conventional radiosensitizers that rely on high-Z effects or DNA-targeted mechanisms, SCNPs potentiate radiation-induced cellular damage by perturbing ion homeostasis. Importantly, SCNPs by elevating intracellular sodium levels reverse the sodium/calcium exchanger (NCX), leading to calcium influx. This calcium surge not only amplifies radiation-induced cancer cell death but also activates the cGAS-STING pathway, leading to the production of type I interferons. In syngeneic head and neck cancer models, SCNPs significantly improve tumor control and long-term survival in combination with radiation, without inducing detectable toxicity. Mechanistic studies reveal that these therapeutic benefits ar","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-06-03T21:16:39.956Z","creation":"2026-05-01T03:10:52.879Z"},"accession":"S-EPMC12464967","cross_references":{"pubmed":["40947651"],"doi":["10.1021/acs.nanolett.5c03022"]}}