ID | 110665 |
Author |
Yano, Seiji
Third Department of Internal Medicine, The University of Tokushima School of Medicine
Yanagawa, Hiroaki
Third Department of Internal Medicine, The University of Tokushima School of Medicine
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Hanibuchi, Masaki
Third Department of Internal Medicine, The University of Tokushima School of Medicine
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Pai, Kalpana
Third Department of Internal Medicine, The University of Tokushima School of Medicine
Nishioka, Yasuhiko
Third Department of Internal Medicine, The University of Tokushima School of Medicine
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Tsuruo, Takashi
Institute of Molecular and Cellular Biosciences, The University of Tokyo
Sone, Saburo
Third Department of Internal Medicine, The University of Tokushima School of Medicine
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Keywords | multidrug resistance
P-glycoprotein
ganglioside GM2
ADCC
cyclosporin A
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Content Type |
Journal Article
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Description | A P-glycoprotein (P-gp) inhibitor, cyclosporin A (CsA) was found to enhance the susceptibility of multidrug resistant (MDR) cancer cells to anti-P-gp antibody-dependent cellular cytolysis (ADCC) by monocytes, but the exact mechanism is unknown. In this study, we examined whether CsA enhanced the susceptibility of MDR cells through its inhibitory effect of P-gp function by using anti-ganglioside GM2 (GM2) monoclonal antibody (Ab), KM966, instead of anti-P-gp Ab, MRK16. Monocyte-ADCC induced by both KM966 and MRK16 against P-gp positive human MDR ovarian cancer cells was significantly augmented by addition of CsA. KM966, but not MRK16, induced monocyte-ADCC against P-gp negative human ovarian cancer cells and CsA enhanced this ADCC activity, indicating that suppressive effect of P-gp function by CsA was not essential to the enhancement of ADCC. Moreover, pretreatment of tumor cells with CsA augmented their susceptibility to monocyte-ADCC irrespective of P-gp expression. Interestingly, KM966 or MRK16 induced monocyte-ADCC against various human lung cancer cells expressing either GM2 or P-gp, but CsA did not affect these ADCC. These findings suggest that CsA may enhance the susceptibility to the monocyte-ADCC of ovarian cancer cells, but not of lung cancer cells, irrespective of its suppressive effect of P-gp function.
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Journal Title |
The journal of medical investigation : JMI
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ISSN | 13431420
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NCID | AA11166929
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Volume | 44
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Issue | 3-4
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Start Page | 185
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End Page | 191
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Sort Key | 185
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Published Date | 1998
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EDB ID | |
FullText File | |
language |
eng
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TextVersion |
Publisher
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departments |
University Hospital
Medical Sciences
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