The antitumor effects of methyl-β-cyclodextrin against primary effusion lymphoma via the depletion of cholesterol from lipid rafts

  • Biochem Biophys Res Commun. 2014 Dec 12;455(3-4):285-9. doi: 10.1016/j.bbrc.2014.11.006.
Kumiko Gotoh  1 ,  Ryusho Kariya  2 ,  Md Masud Alam  2 ,  Kouki Matsuda  2 ,  Shinichiro Hattori  2 ,  Yuki Maeda  3 ,  Keiichi Motoyama  3 ,  Akihiro Kojima  4 ,  Hidetoshi Arima  3 ,  Seiji Okada  5
Affiliations
  • 1. Division of Hematopoiesis, Center for AIDS Research, Kumamoto University, Kumamoto, Japan; Radioisotope Center, Institute of Resource Development and Analysis (IRDA), Kumamoto University, Kumamoto, Japan.
  • 2. Division of Hematopoiesis, Center for AIDS Research, Kumamoto University, Kumamoto, Japan.
  • 3. Department of Physical Pharmaceutics, Graduate School of Pharmaceutical Sciences, Kumamoto University, Kumamoto, Japan.
  • 4. Radioisotope Center, Institute of Resource Development and Analysis (IRDA), Kumamoto University, Kumamoto, Japan.
  • 5. Division of Hematopoiesis, Center for AIDS Research, Kumamoto University, Kumamoto, Japan. Electronic address: [email protected].
PMID: 25446086 DOI: 10.1016/j.bbrc.2014.11.006
Abstract

Primary effusion lymphoma (PEL) is a subtype of aggressive and chemotherapy-resistant non-Hodgkin lymphoma that occurs predominantly in patients with advanced AIDS. In this study, we examined the antitumor activity of methyl-β-cyclodextrin (M-β-CyD) in vitro and in vivo. M-β-CyD quickly induced caspase-dependent Apoptosis in PEL cells via Cholesterol depletion from the plasma membrane. In a PEL xenograft mouse model, M-β-CyD significantly inhibited the growth and invasion of PEL cells without apparent adverse effects. These results strongly suggest that M-β-CyD has the potential to be an effective antitumor agent against PEL.

Keywords
Apoptosis; Cholesterol; Methyl-β-cyclodextrin; Mice model; Plasma membrane; Primary effusion lymphoma.
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