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<p>As a well-known cancer risk region, the <i>8q24</i> locus is frequently amplified in a variety of solid tumors. Here we identify a pseudogene-derived oncogenic lncRNA, <i>ZNF252P</i>, which is upregulated in a variety of cancer types by copy number gain as well as <i>c-Myc</i>-mediated transcriptional activation. Mechanistically, <i>ZNF252P</i> binds and drives “phase separation” of HNRNPK and ILF3 protein in the nucleus and cytoplasm, respectively, to transcriptionally and posttranscriptionally activate <i>c-Myc</i>, thus forming a <i>c-Myc</i>/<i>ZNF252P</i>/<i>c-Myc</i> positive feedback loop. These findings expand the understanding of the relationship between genomic instability in the <i>8q24</i> region and tumorigenesis and clarify a regulatory mechanism involved in transcription and posttranscription from the perspective of RNA-mediated nuclear and cytoplasmic protein phase separation, which sheds light on the dialogue with the driver oncogene <i>c-Myc</i>. The pivotal regulatory axis of <i>ZNF252P</i>/<i>c-Myc</i> has potential as a promising biomarker and therapeutic target in cancer development.</p>

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8q24 derived ZNF252P promotes tumorigenesis by driving phase separation to activate c-Myc mediated feedback loop

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年2月26日

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  • Tianyu Qu,
  • Chang Zhang,
  • Xiyi Lu,
  • Jiali Dai,
  • Xuezhi He,
  • Wei Li,
  • Liang Han,
  • Dandan Yin,
  • Erbao Zhang

摘要

As a well-known cancer risk region, the 8q24 locus is frequently amplified in a variety of solid tumors. Here we identify a pseudogene-derived oncogenic lncRNA, ZNF252P, which is upregulated in a variety of cancer types by copy number gain as well as c-Myc-mediated transcriptional activation. Mechanistically, ZNF252P binds and drives “phase separation” of HNRNPK and ILF3 protein in the nucleus and cytoplasm, respectively, to transcriptionally and posttranscriptionally activate c-Myc, thus forming a c-Myc/ZNF252P/c-Myc positive feedback loop. These findings expand the understanding of the relationship between genomic instability in the 8q24 region and tumorigenesis and clarify a regulatory mechanism involved in transcription and posttranscription from the perspective of RNA-mediated nuclear and cytoplasmic protein phase separation, which sheds light on the dialogue with the driver oncogene c-Myc. The pivotal regulatory axis of ZNF252P/c-Myc has potential as a promising biomarker and therapeutic target in cancer development.