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Response of head and neck epithelial cells to a DNA damage-differentiation checkpoint involving polyploidization

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Autores de IDIVAL

Autores ajenos al IDIVAL

  • Sanz-Gomez, N
  • Freije, A
  • Ceballos, L
  • Obeso, S
  • Sanz, JR

Unidades

Abstract

Background Squamous epithelia of the head and neck undergo continuous cell renewal and are continuously exposed to mutagenic hazard, the main cause of cancer. How they maintain homeostasis upon cell cycle deregulation is unclear. Methods To elucidate how head and neck epithelia respond to cell cycle stress, we studied human keratinocytes from various locations (oral mucosa, tonsil, pharynx, larynx, and trachea). We made use of genotoxic or mitotic drugs (doxorubicin [DOXO], paclitaxel, and nocodazole), or chemical inhibitors of the mitotic checkpoint kinases, Aurora B and polo-like-1. We further tested the response to inactivation of p53, ectopic cyclin E, or to the chemical carcinogen 7,12-dimethylbenz[a]anthracene (DMBA). Results All treatments provoked DNA damage or mitosis impairment and strikingly triggered squamous differentiation and polyploidization, resulting in irreversible loss of clonogenic capacity. Conclusion Keratinocytes from head and neck epithelia share a cell-autonomous squamous DNA damage-differentiation response that is common to the epidermis and might continuously protect them from cancer.

© 2018 Wiley Periodicals, Inc.

Datos de la publicación

ISSN/ISSNe:
1043-3074, 1097-0347

HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND NECK  WILEY

Tipo:
Article
Páginas:
2487-2497

Citas Recibidas en Web of Science: 14

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Keywords

  • aneuploidy; DNA damage; genomic instability; head and neck; squamous cell carcinoma (SCC)

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