Quantification of beta-galactosidase activity as a marker of radiation-driven cellular senescence

Vanessa Klapp, Norma Bloy, Giulia Petroni*, Mara De Martino

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

Abstract

Cellular senescence is a permanent state of cell cycle arrest that can be triggered by different stressors, including cancer treatments (the so-called “therapy-induced senescence”), such as radiation therapy (RT). Although senescent cells do not proliferate, they remain metabolically active and play a critical role in tumor progression, metastasis, and response to therapy. Therefore, investigating the induction of cellular senescence upon RT treatment is a critical read out for investigating RT efficacy or combinatorial strategies in cancer research. Senescent cells are characterized by a plethora of markers, including an increased content and activity of lysosomes, which can be detected by the activity of the lysosomal enzyme senescence-associated β-galactosidase. In this chapter, we present a protocol for the gold standard cytochemical method for quantification of the activity of the senescence-associated β-galactosidase in irradiated murine breast cancer cells in vitro.

Original languageEnglish
Title of host publicationRadiation Oncology and Radiotherapy
EditorsJeffrey Kraynak, Lorenzo Galluzzi, Ariel E Marciscano, Ai Sato
PublisherAcademic Press Inc.
Pages113-126
Number of pages14
Volume174
ISBN (Print)9780323899475
DOIs
Publication statusPublished - 2023
Externally publishedYes

Publication series

NameMethods in Cell Biology
Volume174
ISSN (Print)0091-679X

Keywords

  • Breast cancer
  • Cell cycle arrest
  • DNA damage
  • SASP
  • TS/A

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