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<p>The MYB-related transcription factor and partner of profilin (MYPOP or p42POP) is a ubiquitously expressed yet understudied protein recently identified as a restriction factor of oncogenic human papillomaviruses (HPV) and proposed tumor suppressor. Here we show that in HPV-transformed cervical cancer cells, MYPOP induces alterations in cell morphology, silences viral and cellular oncogenes including <i>E6</i> and <i>MYC</i>, and stimulates the release of the cancer-killing cytokine interleukin-24. Transcriptomic and live-cell analyses reveal a rapid G1/S-phase arrest followed by loss of viable cervical cancer cells and induction of apoptosis. Moreover, MYPOP expression is broadly diminished across multiple human cancers, and its re-expression by both DNA- and mRNA-gene transfer markedly suppresses tumor cell proliferation while sparing normal epidermal keratinocytes. Similarly, murine Mypop inhibits mouse cancer cell growth. Collectively, our findings identify MYPOP as a selective suppressor of tumor cell proliferation across species in vitro and point to its potential relevance for future therapeutic investigation.</p>

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The MYB-related transcription factor MYPOP acts as a selective regulator of cancer cell growth

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月19日

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  • Johannes Strunk,
  • Alena Hüppner,
  • Mahwish Sial,
  • Matthias Plath,
  • Mika B. Sheriff,
  • Sascha Wagner,
  • Kirsten Freitag,
  • Snježana Mikuličić,
  • Tatjana Döring,
  • Tobias Bopp,
  • Matthias Klein,
  • Krishnaraj Rajalingam,
  • Gregory Harms,
  • Federico Marini,
  • Annekathrin S. Nedwed,
  • Thomas Hankeln,
  • Carina Osterhof,
  • Marc A. Schneider,
  • Alina Henrich,
  • Andrea Nubbemeyer,
  • Martin Suchan,
  • Silke Brill,
  • Mario Perkovic,
  • Barbara Schrörs,
  • Sebastian Kreiter,
  • Anne Kölsch,
  • Mustafa Diken,
  • Luise Florin

摘要

The MYB-related transcription factor and partner of profilin (MYPOP or p42POP) is a ubiquitously expressed yet understudied protein recently identified as a restriction factor of oncogenic human papillomaviruses (HPV) and proposed tumor suppressor. Here we show that in HPV-transformed cervical cancer cells, MYPOP induces alterations in cell morphology, silences viral and cellular oncogenes including E6 and MYC, and stimulates the release of the cancer-killing cytokine interleukin-24. Transcriptomic and live-cell analyses reveal a rapid G1/S-phase arrest followed by loss of viable cervical cancer cells and induction of apoptosis. Moreover, MYPOP expression is broadly diminished across multiple human cancers, and its re-expression by both DNA- and mRNA-gene transfer markedly suppresses tumor cell proliferation while sparing normal epidermal keratinocytes. Similarly, murine Mypop inhibits mouse cancer cell growth. Collectively, our findings identify MYPOP as a selective suppressor of tumor cell proliferation across species in vitro and point to its potential relevance for future therapeutic investigation.