{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,12]],"date-time":"2026-06-12T17:10:57Z","timestamp":1781284257665,"version":"3.54.1"},"reference-count":28,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2023,5,8]],"date-time":"2023-05-08T00:00:00Z","timestamp":1683504000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81771053"],"award-info":[{"award-number":["81771053"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Oral Diseases"],"published-print":{"date-parts":[[2024,4]]},"abstract":"Abstract<\/jats:title>\n \n Objective<\/jats:title>\n \n The aim of this study was to explore the regulatory effect of\n RUNX2<\/jats:italic>\n mutation on dental follicle cells (DFCs) senescence and clarify the underlying mechanism. This study aimed to explore the basis for a novel mechanism of delayed permanent tooth eruption in cleidocranial dysplasia (CCD) patients.\n <\/jats:p>\n <\/jats:sec>\n \n Materials and Methods<\/jats:title>\n Dental follicles were collected from a CCD patient and healthy controls. Senescence\u2010associated \u03b2\u2010galactosidase (SA\u2010\u03b2\u2010gal) staining, Ki67 staining, cell cycle assays, and senescence\u2010related gene and protein expression assays were performed to assess DFCs senescence. Western blotting was performed to detect the activation of mitogen\u2010activated protein kinase (MAPK) signalling pathways, and the molecular mechanism underlying RUNX2 regulating in DFCs senescence was explored.<\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n RUNX2<\/jats:italic>\n mutation inhibited the cellular senescence of DFCs from the CCD patient compared with healthy controls. Ki67 staining showed that mutant RUNX2 promoted DFCs proliferation, and cell cycle assays revealed that the healthy control\u2010derived DFCs arrested at G1 phase.\n RUNX2<\/jats:italic>\n mutation significantly downregulated senescence\u2010associated gene and protein expression.\n RUNX2<\/jats:italic>\n mutation suppressed ERK signalling pathway activation, an ERK inhibitor decreased healthy control\u2010derived DFCs senescence, and an ERK activator promoted CCD patient\u2010derived DFCs senescence.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n RUNX2<\/jats:italic>\n mutation delayed DFCs senescence through the ERK signalling pathway, which may be responsible for delayed permanent tooth eruption in CCD patients.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/odi.14607","type":"journal-article","created":{"date-parts":[[2023,5,8]],"date-time":"2023-05-08T07:25:44Z","timestamp":1683530744000},"page":"1337-1349","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["\n RUNX2<\/i>\n <\/scp>\n mutation inhibits the cellular senescence of dental follicle cells via\n ERK<\/scp>\n signalling pathway"],"prefix":"10.1111","volume":"30","author":[{"given":"LingLi","family":"Ji","sequence":"first","affiliation":[{"name":"Department of Preventive Dentistry Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices Beijing PR 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