APAF-1-ALT, a novel alternative splicing form of APAF-1, potentially causes impeded ability of undergoing DNA damage-induced apoptosis in the LNCaP human prostate cancer cell line

Takenori Ogawa, Kiyoto Shiga, Sho Hashimoto, Toshimitsu Kobayashi, Akira Horii, Toru Furukawa

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

We have found a novel alternative splicing product of the apoptotic protease activating factor 1 (APAF-1), termed APAF-1-ALT, in the LNCaP human prostate cancer cell line. APAF-1-ALT harbors the caspase recruitment domain and an incomplete CED-4 like/ATPase domain, but lacks the WD-40 repeat units. The LNCaP cell expressed the full-length APAF-1 weakly and APAF-1-ALT rather abundantly, especially after mycoplasma infection. LNCaP underwent a retarded DNA damage-induced apoptosis, which was independent of caspase 9 activity. APAF-1-ALT functioned less effectively in inducing apoptosis than did APAF-1-XL, the full-length APAF-1, in transient transfection. Moreover, APAF-1-ALT interfered with APAF-1-XL's ability to induce apoptosis in transient double transfection experiment. These results indicate that APAF-1-ALT is a molecule that is deficient and impeded for mediating apoptosis and that it may contribute to the resistance to DNA damage-induced treatment observed in LNCaP.

Original languageEnglish
Pages (from-to)537-543
Number of pages7
JournalBiochemical and biophysical research communications
Volume306
Issue number2
DOIs
Publication statusPublished - 2003 Jun 27

Keywords

  • APAF-1
  • APAF-1-ALT
  • APAF-1-XL
  • Alternative splicing
  • Apoptosis
  • CARD
  • Caspase 9
  • Prostate cancer

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Fingerprint Dive into the research topics of 'APAF-1-ALT, a novel alternative splicing form of APAF-1, potentially causes impeded ability of undergoing DNA damage-induced apoptosis in the LNCaP human prostate cancer cell line'. Together they form a unique fingerprint.

  • Cite this