Scholarlink

<p>Breast cancer has become the main cause threatening women’s health. RNA editing is one of the most important mechanisms for modifying genetic information. This study explained the relationship between A-to-I RNA edited miR-3664-5p and malignant phenotype of breast cancer. The results showed that high editing level of miR-3664-5p in breast cancer, which was related to tumor stage, recurrence and prognosis of breast cancer patients. ADAR perturbation experiments demonstrated that ADAR1 is the key enzyme regulating miR-3664-5p editing in breast cancer. A series of in vitro assays revealed that miR-3664-5p functioned as a tumor suppressor in breast cancer, but ed-miR-3664-5p promoted breast cancer development. Mechanically, dual-luciferase reporter assay confirmed that ed-miR-3664-5p directly targets <i>LONP2</i>, yet wt-miR-3664-5p loss this binding site. ChIP assay proved that PKM2 was enriched in the transcriptional regulatory region of LONP2 gene. Seahorse XFe analysis showed that <i>LONP2</i> knockdown strengthened glycolysis in breast cancer. Xenograft assay also demonstrated that edited miR-3664-5p affected glycolysis in breast cancer through the regulation of <i>LONP2</i>. In conclusion, A-to-I RNA editing endows miR-3664-5p with carcinogenicity in breast cancer through modulating <i>LONP2</i> mediated glycolysis.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

A-to-I RNA Editing Endows miR-3664-5p with Carcinogenicity in Breast Cancer Through Modulating LONP2 Mediated Glycolysis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月16日

查看全文
  • Yajing Han,
  • Xueli Wei,
  • Xuesen Zhang,
  • Jianjun Wu,
  • Fan Wang

摘要

Breast cancer has become the main cause threatening women’s health. RNA editing is one of the most important mechanisms for modifying genetic information. This study explained the relationship between A-to-I RNA edited miR-3664-5p and malignant phenotype of breast cancer. The results showed that high editing level of miR-3664-5p in breast cancer, which was related to tumor stage, recurrence and prognosis of breast cancer patients. ADAR perturbation experiments demonstrated that ADAR1 is the key enzyme regulating miR-3664-5p editing in breast cancer. A series of in vitro assays revealed that miR-3664-5p functioned as a tumor suppressor in breast cancer, but ed-miR-3664-5p promoted breast cancer development. Mechanically, dual-luciferase reporter assay confirmed that ed-miR-3664-5p directly targets LONP2, yet wt-miR-3664-5p loss this binding site. ChIP assay proved that PKM2 was enriched in the transcriptional regulatory region of LONP2 gene. Seahorse XFe analysis showed that LONP2 knockdown strengthened glycolysis in breast cancer. Xenograft assay also demonstrated that edited miR-3664-5p affected glycolysis in breast cancer through the regulation of LONP2. In conclusion, A-to-I RNA editing endows miR-3664-5p with carcinogenicity in breast cancer through modulating LONP2 mediated glycolysis.