Min Sun, Yanrong Ma, Jing Wan, Bingli Zheng, Zhenfeng Shi, Jiuzhi Li
{"title":"DNMT3B通过介导LRP1B启动子的超甲基化促进嗜铬细胞瘤的进展。","authors":"Min Sun, Yanrong Ma, Jing Wan, Bingli Zheng, Zhenfeng Shi, Jiuzhi Li","doi":"10.1186/s13072-025-00592-8","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Pheochromocytoma (Pheo) represents a potential metastatic neuroendocrine tumor. As a tumor suppressor gene, LRP1B is involved in the regulation of tumor progression. However, the precise regulatory mechanism of LRP1B in Pheo remains elusive.</p><p><strong>Methods: </strong>RT-QPCR, western blot and immunohistochemistry (IHC) were used to identify the expression levels of DNMT3B and LRP1B. Biochemistry assays including luciferase and ChIP were utilized to detect the interaction between the methyltransferase DNMT3B and LRP1B promoter. LRP1B or DNMT3B were knock-down in Pheo cell line by shRNAs. Functional experiments including clonal formation, migration, and in vivo transplantation were performed to evaluate the regulation of LRP1B or DNMT3B on tumor growth.</p><p><strong>Results: </strong>LRP1B was down-regulated, while DNMT3B was up-regulated in Pheo.Overexpression of LRP1B or inhibition of DNMT3B inhibited the progress of Pheo. DNMT3B was responsible for the hypermethylation of LRP1B promoter in Pheo. At the same time, overexpression of DNMT3B reversed the inhibitory effect of overexpression of LRP1B on Pheo progression.</p><p><strong>Conclusion: </strong>DNMT3B mediated the hypermethylation of the tumor suppressive gene LRP1B and promotes Pheo progression.</p>","PeriodicalId":49253,"journal":{"name":"Epigenetics & Chromatin","volume":"18 1","pages":"29"},"PeriodicalIF":4.2000,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12063281/pdf/","citationCount":"0","resultStr":"{\"title\":\"DNMT3B promotes the progression of pheochromocytoma by mediating the hypermethylation of LRP1B promoter.\",\"authors\":\"Min Sun, Yanrong Ma, Jing Wan, Bingli Zheng, Zhenfeng Shi, Jiuzhi Li\",\"doi\":\"10.1186/s13072-025-00592-8\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Pheochromocytoma (Pheo) represents a potential metastatic neuroendocrine tumor. As a tumor suppressor gene, LRP1B is involved in the regulation of tumor progression. However, the precise regulatory mechanism of LRP1B in Pheo remains elusive.</p><p><strong>Methods: </strong>RT-QPCR, western blot and immunohistochemistry (IHC) were used to identify the expression levels of DNMT3B and LRP1B. Biochemistry assays including luciferase and ChIP were utilized to detect the interaction between the methyltransferase DNMT3B and LRP1B promoter. LRP1B or DNMT3B were knock-down in Pheo cell line by shRNAs. Functional experiments including clonal formation, migration, and in vivo transplantation were performed to evaluate the regulation of LRP1B or DNMT3B on tumor growth.</p><p><strong>Results: </strong>LRP1B was down-regulated, while DNMT3B was up-regulated in Pheo.Overexpression of LRP1B or inhibition of DNMT3B inhibited the progress of Pheo. DNMT3B was responsible for the hypermethylation of LRP1B promoter in Pheo. At the same time, overexpression of DNMT3B reversed the inhibitory effect of overexpression of LRP1B on Pheo progression.</p><p><strong>Conclusion: </strong>DNMT3B mediated the hypermethylation of the tumor suppressive gene LRP1B and promotes Pheo progression.</p>\",\"PeriodicalId\":49253,\"journal\":{\"name\":\"Epigenetics & Chromatin\",\"volume\":\"18 1\",\"pages\":\"29\"},\"PeriodicalIF\":4.2000,\"publicationDate\":\"2025-05-09\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12063281/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Epigenetics & Chromatin\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1186/s13072-025-00592-8\",\"RegionNum\":2,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"GENETICS & HEREDITY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Epigenetics & Chromatin","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1186/s13072-025-00592-8","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}
DNMT3B promotes the progression of pheochromocytoma by mediating the hypermethylation of LRP1B promoter.
Background: Pheochromocytoma (Pheo) represents a potential metastatic neuroendocrine tumor. As a tumor suppressor gene, LRP1B is involved in the regulation of tumor progression. However, the precise regulatory mechanism of LRP1B in Pheo remains elusive.
Methods: RT-QPCR, western blot and immunohistochemistry (IHC) were used to identify the expression levels of DNMT3B and LRP1B. Biochemistry assays including luciferase and ChIP were utilized to detect the interaction between the methyltransferase DNMT3B and LRP1B promoter. LRP1B or DNMT3B were knock-down in Pheo cell line by shRNAs. Functional experiments including clonal formation, migration, and in vivo transplantation were performed to evaluate the regulation of LRP1B or DNMT3B on tumor growth.
Results: LRP1B was down-regulated, while DNMT3B was up-regulated in Pheo.Overexpression of LRP1B or inhibition of DNMT3B inhibited the progress of Pheo. DNMT3B was responsible for the hypermethylation of LRP1B promoter in Pheo. At the same time, overexpression of DNMT3B reversed the inhibitory effect of overexpression of LRP1B on Pheo progression.
Conclusion: DNMT3B mediated the hypermethylation of the tumor suppressive gene LRP1B and promotes Pheo progression.
期刊介绍：
Epigenetics & Chromatin is a peer-reviewed, open access, online journal that publishes research, and reviews, providing novel insights into epigenetic inheritance and chromatin-based interactions. The journal aims to understand how gene and chromosomal elements are regulated and their activities maintained during processes such as cell division, differentiation and environmental alteration.
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