{"title":"肽eng00000232259 - orf通过促进自噬抑制胶质瘤细胞的增殖和迁移。","authors":"Jiaqi Zhang , Gangao Wei , Baoshun Du , Zhenguo Cheng , Zheying Zhang","doi":"10.1016/j.brainres.2025.149942","DOIUrl":null,"url":null,"abstract":"<div><div>Glioma is a malignant brain tumor in which the lncRNA ENSG00000232259 is significantly upregulated. Bioinformatics predictions suggest that it may encode the polypeptide ENSG00000232259-ORF, but the biological function and mechanisms of this polypeptide in glioma remain unclear. Gene expression and correlation analyses were conducted using the GEPIA database, combined with GetORF to predict the polypeptide-coding potential, and Western blot was employed to validate the expression of ENSG00000232259-ORF. Functional experiments demonstrated that this polypeptide significantly inhibits glioma cell proliferation and migration, as evidenced by CCK8, colony formation, Transwell, and scratch assays, and this effect is independent of its parent lncRNA. Mechanistically, ENSG00000232259-ORF promotes autophagy by upregulating ATG3 expression, manifested by increased levels of LC3B and decreased P62. Knockdown of ATG3 reversed the inhibitory effects of the polypeptide on cell proliferation and migration. These findings reveal that ENSG00000232259-ORF suppresses glioma progression by activating the autophagy pathway, providing a potential new target for tumor therapy.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1866 ","pages":"Article 149942"},"PeriodicalIF":2.6000,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The peptide ENSG00000232259-ORF inhibits glioma cell proliferation and migration by promoting autophagy\",\"authors\":\"Jiaqi Zhang , Gangao Wei , Baoshun Du , Zhenguo Cheng , Zheying Zhang\",\"doi\":\"10.1016/j.brainres.2025.149942\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Glioma is a malignant brain tumor in which the lncRNA ENSG00000232259 is significantly upregulated. Bioinformatics predictions suggest that it may encode the polypeptide ENSG00000232259-ORF, but the biological function and mechanisms of this polypeptide in glioma remain unclear. Gene expression and correlation analyses were conducted using the GEPIA database, combined with GetORF to predict the polypeptide-coding potential, and Western blot was employed to validate the expression of ENSG00000232259-ORF. Functional experiments demonstrated that this polypeptide significantly inhibits glioma cell proliferation and migration, as evidenced by CCK8, colony formation, Transwell, and scratch assays, and this effect is independent of its parent lncRNA. Mechanistically, ENSG00000232259-ORF promotes autophagy by upregulating ATG3 expression, manifested by increased levels of LC3B and decreased P62. Knockdown of ATG3 reversed the inhibitory effects of the polypeptide on cell proliferation and migration. These findings reveal that ENSG00000232259-ORF suppresses glioma progression by activating the autophagy pathway, providing a potential new target for tumor therapy.</div></div>\",\"PeriodicalId\":9083,\"journal\":{\"name\":\"Brain Research\",\"volume\":\"1866 \",\"pages\":\"Article 149942\"},\"PeriodicalIF\":2.6000,\"publicationDate\":\"2025-09-08\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Brain Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0006899325005050\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Brain Research","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0006899325005050","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
The peptide ENSG00000232259-ORF inhibits glioma cell proliferation and migration by promoting autophagy
Glioma is a malignant brain tumor in which the lncRNA ENSG00000232259 is significantly upregulated. Bioinformatics predictions suggest that it may encode the polypeptide ENSG00000232259-ORF, but the biological function and mechanisms of this polypeptide in glioma remain unclear. Gene expression and correlation analyses were conducted using the GEPIA database, combined with GetORF to predict the polypeptide-coding potential, and Western blot was employed to validate the expression of ENSG00000232259-ORF. Functional experiments demonstrated that this polypeptide significantly inhibits glioma cell proliferation and migration, as evidenced by CCK8, colony formation, Transwell, and scratch assays, and this effect is independent of its parent lncRNA. Mechanistically, ENSG00000232259-ORF promotes autophagy by upregulating ATG3 expression, manifested by increased levels of LC3B and decreased P62. Knockdown of ATG3 reversed the inhibitory effects of the polypeptide on cell proliferation and migration. These findings reveal that ENSG00000232259-ORF suppresses glioma progression by activating the autophagy pathway, providing a potential new target for tumor therapy.
期刊介绍:
An international multidisciplinary journal devoted to fundamental research in the brain sciences.
Brain Research publishes papers reporting interdisciplinary investigations of nervous system structure and function that are of general interest to the international community of neuroscientists. As is evident from the journals name, its scope is broad, ranging from cellular and molecular studies through systems neuroscience, cognition and disease. Invited reviews are also published; suggestions for and inquiries about potential reviews are welcomed.
With the appearance of the final issue of the 2011 subscription, Vol. 67/1-2 (24 June 2011), Brain Research Reviews has ceased publication as a distinct journal separate from Brain Research. Review articles accepted for Brain Research are now published in that journal.