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Driving effect of P16 methylation on telomerase reverse transcriptase-mediated immortalization and transformation of

Xuehong Zhang1, Paiyun Li2,3, Ying Gan1

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P16 methylation, driven by telomerase reverse transcriptase (TERT), promotes normal human cell immortalization and transformation, potentially contributing to cancer development. This study provides experimental evidence for P16

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Area of Science:

  • Epigenetics and Cancer Biology
  • Cellular Immortalization and Transformation

Background:

  • P16 gene inactivation and telomerase reverse transcriptase (TERT) amplification are common in human cancers.
  • Epigenetic changes like P16 methylation are implicated in cancer development, but direct causal evidence is limited.

Purpose of the Study:

  • To provide experimental evidence that P16 methylation directly drives cancer development.
  • To investigate the role of P16 methylation in TERT-mediated cellular processes.

Main Methods:

  • Utilized a zinc finger protein-based P16-specific DNA methyltransferase (P16-Dnmt) vector with a
  • Tet-On
  • switch to induce P16 methylation in human fibroblasts (CCD-18Co cells).
  • Assessed cell immortalization and transformation using battery assays.
  • Employed cell subcloning and DNA barcoding to track cellular evolution.

Main Results:

  • P16 methylation alone promoted proliferation and extended cell lifespan but did not induce immortalization.
  • Combined P16 methylation and TERT expression led to cell immortalization, loss of contact inhibition, and anchorage-independent growth (cell transformation).
  • TERT-expressing cells with P16 methylation exhibited enhanced subclone formation capacity and greater population diversity compared to TERT cells alone.

Conclusions:

  • P16 methylation is a key driver of TERT-mediated immortalization and transformation in normal human cells.
  • These findings suggest a direct mechanism by which epigenetic alterations contribute to cancer development.