Crosstalk between tumor suppressors p53 and PKCδ: Execution of the intrinsic apoptotic pathways

Nurmaa Dashzeveg, Kiyotsugu Yoshida*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

15 Scopus citations


p53 and PKCδ are tumor suppressors that execute apoptotic mechanisms in response to various cellular stresses. p53 is a transcription factor that is frequently mutated in human cancers; it regulates apoptosis in transcription-dependent and -independent ways in response to genotoxic stresses. PKCδ is a serine/threonine protein kinase and mutated in human cancers. Available evidence shows that PKCδ activates p53 by direct and/or indirect mechanisms. Moreover, PKCδ is also implicated in the transcriptional regulation of p53 in response to DNA damage. Recent findings demonstrated that p53, in turn, binds onto the PKCδ promoter and induces its expression upon DNA damage to facilitate apoptosis. Both p53 and PKCδ are associated with the apoptotic mechanisms in the mitochondria by regulating Bcl-2 family proteins to provide mitochondrial outer membrane permeabilization. This review discusses the crosstalk between p53 and PKCδ in the context of apoptotic cell death and cancer therapy.

Original languageEnglish (US)
Pages (from-to)158-163
Number of pages6
JournalCancer Letters
Issue number2
StatePublished - Jul 28 2016


  • Apoptosis
  • DNA damage
  • Mitochondrial outer membrane permeabilization
  • P53
  • PKCδ

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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