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Background <p>Pheochromocytoma (Pheo) represents a potential metastatic neuroendocrine tumor. As a tumor suppressor gene, <i>LRP1B</i> is involved in the regulation of tumor progression. However, the precise regulatory mechanism of <i>LRP1B</i> in Pheo remains elusive.</p> Methods <p>RT-QPCR, western blot and immunohistochemistry (IHC) were used to identify the expression levels of <i>DNMT3B</i> and <i>LRP1B</i>. Biochemistry assays including luciferase and ChIP were utilized to detect the interaction between the methyltransferase DNMT3B and <i>LRP1B</i> promoter. <i>LRP1B</i> or <i>DNMT3B</i> 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 <i>LRP1B</i> or DNMT3B on tumor growth.</p> Results <p><i>LRP1B</i> was down-regulated, while <i>DNMT3B</i> was up-regulated in Pheo.Overexpression of <i>LRP1B</i> or inhibition of <i>DNMT3B</i> inhibited the progress of Pheo. DNMT3B was responsible for the hypermethylation of <i>LRP1B</i> promoter in Pheo. At the same time, overexpression of <i>DNMT3B</i> reversed the inhibitory effect of overexpression of <i>LRP1B</i> on Pheo progression.</p> Conclusion <p>DNMT3B mediated the hypermethylation of the tumor suppressive gene <i>LRP1B</i> and promotes Pheo progression.</p>

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DNMT3B promotes the progression of pheochromocytoma by mediating the hypermethylation of LRP1B promoter

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月9日

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  • Min Sun,
  • Yanrong Ma,
  • Jing Wan,
  • Bingli Zheng,
  • Zhenfeng Shi,
  • Jiuzhi Li

摘要

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.