Cell death signaling and anticancer therapy

Lorenzo Galluzzi, Ilio Vitale, Erika Vacchelli, Guido Kroemer

Research output: Contribution to journalArticlepeer-review

Abstract

For a long time, it was commonly believed that efficient anticancer regimens would either trigger the apoptotic demise of tumor cells or induce a permanent arrest in the G1 phase of the cell cycle, i.e., senescence. The recent discovery that necrosis can occur in a regulated fashion and the increasingly more precise characterization of the underlying molecular mechanisms have raised great interest, as non-apoptotic pathways might be instrumental to circumvent the resistance of cancer cells to conventional, pro-apoptotic therapeutic regimens. Moreover, it has been shown that some anticancer regimens engage lethal signaling cascades that can ignite multiple oncosuppressive mechanisms, including apoptosis, necrosis, and senescence. Among these signaling pathways is mitotic catastrophe, whose role as a bona fide cell death mechanism has recently been reconsidered. Thus, anticancer regimens get ever more sophisticated, and often distinct strategies are combined to maximize efficacy and minimize side effects. In this review, we will discuss the importance of apoptosis, necrosis, and mitotic catastrophe in the response of tumor cells to the most common clinically employed and experimental anticancer agents.

Original languageEnglish
Article number00005
JournalFrontiers in Oncology
Volume1
Issue numberMAY
DOIs
Publication statusPublished - 2011

Keywords

  • Caspases
  • Lysosomal membrane permeabilization
  • Mitochondrial membrane permeabilization
  • Necrosome
  • Oncosis
  • Phosphatidylserine
  • Reactive oxygen species
  • RIP1

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Fingerprint

Dive into the research topics of 'Cell death signaling and anticancer therapy'. Together they form a unique fingerprint.

Cite this