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<p>The gene <i>Tfcp2l1</i> has emerged as a central player linking key processes in cancer biology: hypoxia, immortalization, dedifferentiation, and tumor progression. Originally identified for its role in maintaining pluripotency in embryonic stem cells, <i>Tfcp2l1</i> has been found to reappear in various cancers, especially under conditions of low oxygen (hypoxia). Hypoxia, a common feature of solid tumors, triggers the reactivation of developmental genes like <i>Tfcp2l1</i>, enabling cancer cells to dedifferentiate and adopt stem cell-like properties. This dedifferentiation facilitates the immortalization of cells—allowing them to bypass senescence and continue proliferating. <i>Tfcp2l1</i> contributes to this process by regulating transcriptional networks that suppress differentiation and support self-renewal. Its expression correlates with poor prognosis in several cancers, highlighting its potential role in tumor aggressiveness and resistance to therapy. By acting at the intersection of cellular plasticity, stress adaptation, and oncogenic transformation, <i>Tfcp2l1</i> may serve as a molecular bridge linking early developmental programs with malignant behaviors. Understanding how <i>Tfcp2l1</i> integrates signals from hypoxic stress and drives dedifferentiation could uncover new therapeutic targets aimed at reversing or halting tumor progression.</p>

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Tfcp2l1 as a central integrator of hypoxia, dedifferentiation, and tumor progression

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月14日

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  • Cynthia Clemente-González,
  • Amancio Carnero

摘要

The gene Tfcp2l1 has emerged as a central player linking key processes in cancer biology: hypoxia, immortalization, dedifferentiation, and tumor progression. Originally identified for its role in maintaining pluripotency in embryonic stem cells, Tfcp2l1 has been found to reappear in various cancers, especially under conditions of low oxygen (hypoxia). Hypoxia, a common feature of solid tumors, triggers the reactivation of developmental genes like Tfcp2l1, enabling cancer cells to dedifferentiate and adopt stem cell-like properties. This dedifferentiation facilitates the immortalization of cells—allowing them to bypass senescence and continue proliferating. Tfcp2l1 contributes to this process by regulating transcriptional networks that suppress differentiation and support self-renewal. Its expression correlates with poor prognosis in several cancers, highlighting its potential role in tumor aggressiveness and resistance to therapy. By acting at the intersection of cellular plasticity, stress adaptation, and oncogenic transformation, Tfcp2l1 may serve as a molecular bridge linking early developmental programs with malignant behaviors. Understanding how Tfcp2l1 integrates signals from hypoxic stress and drives dedifferentiation could uncover new therapeutic targets aimed at reversing or halting tumor progression.