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Repression of Multiple Myeloma Cell Growth In Vivo by Single-wall Carbon Nanotube (SWCNT)-delivered MALAT1 Antisense Oligos
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Fatty acid synthase is a novel therapeutic target in multiple myeloma

Yutaka Okawa1, Teru Hideshima, Hiroshi Ikeda

  • 1LeBow Institute for Myeloma Therapeutics and Jerome Lipper Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA. yutaka_okawa@dfci.harvard.edu

British Journal of Haematology
|April 16, 2008
PubMed

Insights

Inhibition of fatty acid synthase (FAS) using Cerulenin effectively combats multiple myeloma (MM) by inducing caspase-independent apoptosis and JNK-dependent cytotoxicity. This highlights FAS as a promising new therapeutic target for MM treatment.

Area of Science:

  • Biochemistry
  • Oncology
  • Molecular Biology

Background:

  • Multiple myeloma (MM) is a hematological malignancy characterized by uncontrolled plasma cell proliferation.
  • Survival and growth of MM cells are supported by factors like interleukin-6 and insulin-like growth factor-1.
  • Fatty acid synthase (FAS) plays a crucial role in cancer cell proliferation and survival.

Purpose of the Study:

  • To investigate the biological significance of inhibiting fatty acid synthase (FAS) in multiple myeloma (MM).
  • To evaluate the efficacy of the small molecule inhibitor Cerulenin against MM cells.
  • To elucidate the mechanisms underlying Cerulenin-induced apoptosis and cytotoxicity in MM.

Main Methods:

  • Treatment of MM cell lines and patient cells with Cerulenin.
  • Assessment of cell growth inhibition, apoptosis, and caspase activation.
  • Analysis of endoplasmic reticulum stress response pathways, including the Grp78/IRE1alpha/JNK pathway.
  • Evaluation of synergistic effects with standard MM chemotherapeutic agents.

Main Results:

  • Cerulenin induced significant growth inhibition and apoptosis in MM cells, overcoming survival signals.
  • Apoptosis was primarily caspase-independent, involving up-regulation of apoptosis-inducing factor/endonuclease G.
  • Cerulenin triggered endoplasmic reticulum stress via the Grp78/IRE1alpha/JNK pathway, contributing to cytotoxicity.
  • Cerulenin demonstrated synergistic effects with Bortezomib, Melphalan, and Doxorubicin.

Conclusions:

  • Inhibition of FAS by Cerulenin is a viable strategy against multiple myeloma.
  • Cerulenin induces MM cell death through caspase-independent apoptosis and JNK-dependent cytotoxicity.
  • Targeting FAS represents a novel therapeutic approach for MM with potential synergistic activity with existing treatments.

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