Scholarlink

<p>NR6A1 is a member of the nuclear receptor superfamily of ligand-activated transcription factors and can bind to conserved DNA sequences, acting as a transcriptional repressor. NR6A1 has been reported to promote prostate cancer, gastric cancer, and testicular germ cell tumor progression. In the present study, we confirmed the oncogenic role of NR6A1 in several types of cancer cells, including HeLa, TFK1, and A549 cells, and revealed that NR6A1 knockdown led to a decrease in lung adenocarcinoma cell proliferation, a reduction in glucose consumption, a reduction in lactic acid production, and decreases in ATP levels and mitochondrial membrane potential. Mechanistically, through a series of methods, including bioinformatics analysis, dual-luciferase reporter gene assay, RT-qPCR, Western blot analysis, and functional rescue experiments, we demonstrated that NR6A1 may promote the expression of HK1 by directly suppressing miR-302a, thereby reprogramming tumor cell glycolysis and enhancing lung adenocarcinoma cell growth. In addition, we found that NR6A1 can affect mTOR signaling, suggesting a broader role in tumor metabolism regulation. In summary, our data indicate that NR6A1 plays an oncogenic role by reprogramming glycolysis via the miR-302a/HK1 axis in lung adenocarcinoma.</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

The nuclear receptor NR6A1 plays an oncogenic role through reprogramming glycolysis in tumors

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年11月11日

查看全文
  • Xiaowen Liu,
  • Ye Li,
  • Xinxu Rao,
  • Shun Xie,
  • Zhuoxian Rong,
  • Lifang Yang,
  • Zenghui enghui Mao,
  • Dan Li

摘要

NR6A1 is a member of the nuclear receptor superfamily of ligand-activated transcription factors and can bind to conserved DNA sequences, acting as a transcriptional repressor. NR6A1 has been reported to promote prostate cancer, gastric cancer, and testicular germ cell tumor progression. In the present study, we confirmed the oncogenic role of NR6A1 in several types of cancer cells, including HeLa, TFK1, and A549 cells, and revealed that NR6A1 knockdown led to a decrease in lung adenocarcinoma cell proliferation, a reduction in glucose consumption, a reduction in lactic acid production, and decreases in ATP levels and mitochondrial membrane potential. Mechanistically, through a series of methods, including bioinformatics analysis, dual-luciferase reporter gene assay, RT-qPCR, Western blot analysis, and functional rescue experiments, we demonstrated that NR6A1 may promote the expression of HK1 by directly suppressing miR-302a, thereby reprogramming tumor cell glycolysis and enhancing lung adenocarcinoma cell growth. In addition, we found that NR6A1 can affect mTOR signaling, suggesting a broader role in tumor metabolism regulation. In summary, our data indicate that NR6A1 plays an oncogenic role by reprogramming glycolysis via the miR-302a/HK1 axis in lung adenocarcinoma.