Transcription of the protein kinase C-δ gene is activated by JNK through c-Jun and ATF2 in response to the anticancer agent doxorubicin

Wook Min Byong, Gun Kim Chang, Jesang Ko, Yoongho Lim, Han Lee Young, Young Shin Soon

Research output: Contribution to journalArticle

10 Citations (Scopus)


Expression of protein kinase C-δ (PKCδ) is up-regulated by apoptosis-inducing stimuli. However, very little is known about the signaling pathways that control PKCδ gene transcription. In the present study, we demonstrate that JNK stimulates PKCδ gene expression via c-Jun and ATF2 in response to the anticancer agent doxorubicin (DXR) in mouse lymphocytic leukemia L1210 cells. Luciferase reporter assays showed that DXR-induced activation of the PKCδ promoter was enhanced by ectopic expression of JNK1, c-Jun, or ATF2, whereas it was strongly reduced by expression of dominant negative JNK1 or by treatment with the JNK inhibitor SP600125. Furthermore, point mutations in the core sequence of the c-Jun/ATF2 binding site suppressed DXR-induced activation of the PKCδ promoter. Our results suggest an additional role for a JNK signaling cascade in DXR-induced PKCδ gene expression.

Original languageEnglish
Pages (from-to)686-708
Number of pages23
JournalExperimental and Molecular Medicine
Issue number6
Publication statusPublished - 2008 Dec 31



  • Activating transcription factor 2
  • Apoptosis
  • Doxorubicin
  • JNK mitogen-activated protein kinases
  • Protein kinase C-δ
  • Proto-oncogene proteins c-jun

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Medicine
  • Molecular Biology
  • Clinical Biochemistry

Cite this