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Updated: Feb 22, 2026

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
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NELF prevents transcriptional readthrough into DNA replication zones in cancer cells

Chihiro Nakayama1,2, Qi Fang1, Yasukazu Daigaku3

  • 1Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.

EMBO Reports
|February 20, 2026
PubMed

Insights

Colorectal cancer cells upregulate NELF-C, a negative transcription elongation factor. Its loss disrupts transcription termination, causing conflicts that may block cell cycle progression, revealing NELF as a therapeutic target.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • RNA polymerase II (Pol II) transcription regulation is crucial for cell proliferation.
  • The rewiring of Pol II transcription in cancer for uncontrolled growth is not fully understood.

Purpose of the Study:

  • To investigate the role of NELF-CD in colorectal cancer.
  • To elucidate the function of NELF-C in Pol II transcription and its implications in cancer.

Main Methods:

  • Auxin-dependent protein degradation to remove NELF-C.
  • Nascent transcript sequencing to analyze Pol II transcription.
  • Analysis of transcription termination factors and transcription-replication conflicts.

Main Results:

  • NELF-CD expression is upregulated in colorectal tumors.
  • Acute loss of NELF-C perturbs Pol II transcription termination globally.
  • NELF-C loss drives transcription into DNA replication zones, causing transcription-replication conflicts.

Conclusions:

  • NELF plays a previously unrecognized role in transcription termination.
  • NELF-C dysregulation contributes to cancer progression by inducing transcription-replication conflicts.
  • NELF is a potential therapeutic target for colorectal cancer treatment.
Keywords:
DNA ReplicationNELFRNA Polymerase IITranscription TerminationTranscription-replication Conflict

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