Pengjun Zhou, Wanning Li, Meiyi Ye, Chunlan Chen, Yifei Wang
{"title":"The impact of KIAA1429 on proliferation and invasion in oral cancer via LINC00958 methylation.","authors":"Pengjun Zhou, Wanning Li, Meiyi Ye, Chunlan Chen, Yifei Wang","doi":"10.1177/09603271251369056","DOIUrl":null,"url":null,"abstract":"<p><p>IntroductionThe investigation focused on the function of LINC00958 in the development of oral cancer, as well as the influence of methylation on tumor formation.MethodsTo explore the role of LINC00958, both its overexpression and its methylated form were examined in oral cancer cells. Various assays including CCK-8, transwell, plate cloning, flow cytometry, and EdU staining were utilized to assess the activity, invasion, cloning efficiency, cell cycle progression, and proliferation of the cancer cells. The tumorigenic potential of these cells was evaluated through experiments conducted on immunodeficient mice. Moreover, the methylation status of LINC00958 mediated by the KIAA1429 protein was confirmed using MeRIP-qPCR.ResultsThe study indicated that the overexpression of LINC00958 enhanced the activity, proliferation, and invasive capabilities of oral cancer cells, thereby increasing their tumorigenic potential. In contrast, overexpression of KIAA1429 led to a decrease in the proliferation, invasion, and tumorigenic properties of these cancer cells. Verification of methylation levels indicated that KIAA1429 overexpression resulted in heightened methylation of LINC00958. It was concluded that KIAA1429 diminishes the proliferation, invasion, and tumorigenesis of cancer cells through the methylation of LINC00958.DiscussionThis research provided insights into the role of LINC00958 in oral cancer cells and underscored the impact of methylation, offering a theoretical foundation for improving clinical diagnosis and treatment strategies for oral cancer patients.</p>","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251369056"},"PeriodicalIF":3.2000,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Human & experimental toxicology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1177/09603271251369056","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/8/12 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
IntroductionThe investigation focused on the function of LINC00958 in the development of oral cancer, as well as the influence of methylation on tumor formation.MethodsTo explore the role of LINC00958, both its overexpression and its methylated form were examined in oral cancer cells. Various assays including CCK-8, transwell, plate cloning, flow cytometry, and EdU staining were utilized to assess the activity, invasion, cloning efficiency, cell cycle progression, and proliferation of the cancer cells. The tumorigenic potential of these cells was evaluated through experiments conducted on immunodeficient mice. Moreover, the methylation status of LINC00958 mediated by the KIAA1429 protein was confirmed using MeRIP-qPCR.ResultsThe study indicated that the overexpression of LINC00958 enhanced the activity, proliferation, and invasive capabilities of oral cancer cells, thereby increasing their tumorigenic potential. In contrast, overexpression of KIAA1429 led to a decrease in the proliferation, invasion, and tumorigenic properties of these cancer cells. Verification of methylation levels indicated that KIAA1429 overexpression resulted in heightened methylation of LINC00958. It was concluded that KIAA1429 diminishes the proliferation, invasion, and tumorigenesis of cancer cells through the methylation of LINC00958.DiscussionThis research provided insights into the role of LINC00958 in oral cancer cells and underscored the impact of methylation, offering a theoretical foundation for improving clinical diagnosis and treatment strategies for oral cancer patients.