The EMT transcription factor ZEB1 governs a fitness-promoting but vulnerable DNA replication stress response

Harald Schuhwerk*, Julia Kleemann, Pooja Gupta, Ruthger van Roey, Isabell Armstark, Martina Kreileder, Nora Feldker, Vignesh Ramesh, Yussuf Hajjaj, Kathrin Fuchs, Mousumi Mahapatro, Mojca Hribersek, Marco Volante, Arwin Groenewoud, Felix B. Engel, Paolo Ceppi, Markus Eckstein, Arndt Hartmann, Fabian Müller, Torsten KrollMarc P. Stemmler, Simone Brabletz, Thomas Brabletz

*Corresponding author for this work

Research output: Contribution to journalJournal articleResearchpeer-review

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Abstract

The DNA damage response (DDR) and epithelial-to-mesenchymal transition (EMT) are two crucial cellular programs in cancer biology. While the DDR orchestrates cell-cycle progression, DNA repair, and cell death, EMT promotes invasiveness, cellular plasticity, and intratumor heterogeneity. Therapeutic targeting of EMT transcription factors, such as ZEB1, remains challenging, but tumor-promoting DDR alterations elicit specific vulnerabilities. Using multi-omics, inhibitors, and high-content microscopy, we discover a chemoresistant ZEB1-high-expressing sub-population (ZEB1hi) with co-rewired cell-cycle progression and proficient DDR across tumor entities. ZEB1 stimulates accelerated S-phase entry via CDK6, inflicting endogenous DNA replication stress. However, DDR buildups involving constitutive MRE11-dependent fork resection allow homeostatic cycling and enrichment of ZEB1hi cells during transforming growth factor β (TGF-β)-induced EMT and chemotherapy. Thus, ZEB1 promotes G1/S transition to launch a progressive DDR benefitting stress tolerance, which concurrently manifests a targetable vulnerability in chemoresistant ZEB1hi cells. Our study thus highlights the translationally relevant intercept of the DDR and EMT.

Original languageEnglish
Article number111819
JournalCell Reports
Volume41
Issue number11
ISSN2211-1247
DOIs
Publication statusPublished - 13. Dec 2022

Keywords

  • cancer
  • cell cycle
  • chemoresistance
  • CP: Cancer
  • DNA damage response
  • DNA replication stress
  • epithelial-to-mesenchymal transition
  • heterogeneity
  • MRE11
  • plasticity
  • ZEB1

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