{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Guo D"],"funding":["Science and Technology Commission of Shanghai Municipality","National Natural Science Foundation of China","National Key Research and Development Program of China"],"pagination":["51"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9999509"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(1)"],"pubmed_abstract":["<h4>Background</h4>NK cell is one of innate immune cells and can protect the body from cancer-initiating cells. It has been reported that GPR116 receptor is involved in inflammation and tumors. However, the effect of GPR116 receptor on the NK cells remains largely unclear.<h4>Results</h4>We discovered that GPR116<sup>-/-</sup> mice could efficiently eliminate pancreatic cancer through enhancing the proportion and function of NK cells in tumor. Moreover, the expression of GPR116 receptor was decreased upon the activation of the NK cells. Besides, GPR116<sup>-/-</sup> NK cells showed higher cytotoxicity and antitumor activity in vitro and in vivo by producing more GzmB and IFNγ than wild-type (WT) NK cells. Mechanistically, GPR116 receptor regulated the function of NK cells via Gαq/HIF1α/NF-"],"journal":["Cell & bioscience"],"pubmed_title":["GPR116 receptor regulates the antitumor function of NK cells via Gαq/HIF1α/NF-κB signaling pathway as a potential immune checkpoint."],"pmcid":["PMC9999509"],"funding_grant_id":["21S11906200","2021YFF0702400","201409002900","81771306","81072459"],"pubmed_authors":["Yao J","Ren Y","Zhang L","Zhou Y","Jin C","Ge Y","Jiang W","Gao Y","Lin H","Hui X","Guo D","Yang R","Duan Y"],"additional_accession":[]},"is_claimable":false,"name":"GPR116 receptor regulates the antitumor function of NK cells via Gαq/HIF1α/NF-κB signaling pathway as a potential immune checkpoint.","description":"<h4>Background</h4>NK cell is one of innate immune cells and can protect the body from cancer-initiating cells. It has been reported that GPR116 receptor is involved in inflammation and tumors. However, the effect of GPR116 receptor on the NK cells remains largely unclear.<h4>Results</h4>We discovered that GPR116<sup>-/-</sup> mice could efficiently eliminate pancreatic cancer through enhancing the proportion and function of NK cells in tumor. Moreover, the expression of GPR116 receptor was decreased upon the activation of the NK cells. Besides, GPR116<sup>-/-</sup> NK cells showed higher cytotoxicity and antitumor activity in vitro and in vivo by producing more GzmB and IFNγ than wild-type (WT) NK cells. Mechanistically, GPR116 receptor regulated the function of NK cells via Gαq/HIF1α/NF-","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Mar","modification":"2025-04-22T14:45:17.689Z","creation":"2024-11-13T20:16:58.016Z"},"accession":"S-EPMC9999509","cross_references":{"pubmed":["36895027"],"doi":["10.1186/s13578-023-01005-7"]}}