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Functional interaction between retinoblastoma protein and stress-activated protein kinase in multiple myeloma cells

D Chauhan1, T Hideshima, S Treon

  • 1Department of Adult Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.

Cancer Research
|March 30, 1999
PubMed

Insights

Gamma irradiation triggers apoptosis in multiple myeloma cells by activating stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK). This kinase directly binds and phosphorylates retinoblastoma protein (Rb), mediating cell death.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cellular Biology

Background:

  • Gamma irradiation (IR) induces apoptosis in multiple myeloma (MM).
  • Stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) pathway activation is linked to IR-induced apoptosis in MM.
  • The precise downstream targets of SAPK/JNK in this process remain under investigation.

Purpose of the Study:

  • To investigate the role of retinoblastoma protein (Rb) as a downstream target of SAPK/JNK in IR-induced MM apoptosis.
  • To elucidate the molecular interactions between SAPK/JNK and Rb during gamma irradiation.

Main Methods:

  • In vivo and in vitro association studies to confirm SAPK/JNK and Rb interaction.
  • Far Western blot analysis to verify direct binding of SAPK/JNK to Rb.
  • Site-directed mutagenesis to examine the role of Rb phosphorylation in apoptosis.

Main Results:

  • Gamma irradiation activates SAPK/JNK in MM cells.
  • Activated SAPK/JNK directly binds to Rb both in vivo and in vitro.
  • SAPK/JNK phosphorylates Rb at its COOH terminus domain.
  • Abrogation of the Rb phosphorylation site prevents SAPK/JNK-mediated phosphorylation and IR-induced apoptosis.

Conclusions:

  • Retinoblastoma protein (Rb) is a direct target of SAPK/JNK in multiple myeloma cells.
  • The interaction and phosphorylation of Rb by SAPK/JNK are critical mediators of gamma irradiation-induced apoptosis in MM.

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