A novel strategy inducing autophagic cell death in Burkitt's lymphoma cells with anti-CD19-targeted liposomal rapamycin.
A novel strategy inducing autophagic cell death in Burkitt's lymphoma cells with anti-CD19-targeted liposomal rapamycin.
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DOI:
10.1038/bcj.2014.2
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发表时间:
2014-02-07
影响因子:
12.8
通讯作者:
Kato, J.
中科院分区:
文献类型:
--
作者:
Ono, K.;Sato, T.;Iyama, S.;Tatekoshi, A.;Hashimoto, A.;Kamihara, Y.;Horiguchi, H.;Kikuchi, S.;Kawano, Y.;Takada, K.;Hayashi, T.;Miyanishi, K.;Sato, Y.;Takimoto, R.;Kobune, M.;Kato, J.
Relapsed or refractory Burkitt's lymphoma often has a poor prognosis in spite of intensive chemotherapy that induces apoptotic and/or necrotic death of lymphoma cells. Rapamycin (Rap) brings about autophagy, and could be another treatment. Further, anti-CD19-targeted liposomal delivery may enable Rap to kill lymphoma cells specifically. Rap was encapsulated by anionic liposome and conjugated with anti-CD19 antibody (CD19-GL-Rap) or anti-CD2 antibody (CD2-GL-Rap) as a control. A fluorescent probe Cy5.5 was also liposomized in the same way (CD19 or CD2-GL-Cy5.5) to examine the efficacy of anti-CD19-targeted liposomal delivery into CD19-positive Burkitt's lymphoma cell line, SKW6.4. CD19-GL-Cy5.5 was more effectively uptaken into SKW6.4 cells than CD2-GL-Cy5.5 in vitro. When the cells were inoculated subcutaneously into nonobese diabetic/severe combined immunodeficiency mice, intravenously administered CD19-GL-Cy5.5 made the subcutaneous tumor fluorescent, while CD2-GL-Cy5.5 did not. Further, CD19-GL-Rap had a greater cytocidal effect on not only SKW6.4 cells but also Burkitt's lymphoma cells derived from patients than CD2-GL-Rap in vitro. The specific toxicity of CD19-GL-Rap was cancelled by neutralizing anti-CD19 antibody. The survival period of mice treated with intravenous CD19-GL-Rap was significantly longer than that of mice treated with CD2-GL-Rap after intraperitoneal inoculation of SKW6.4 cells. Anti-CD19-targeted liposomal Rap could be a promising lymphoma cell-specific treatment inducing autophagic cell death.
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影响因子:
12.4
作者:
Nie Y;Ji L;Ding H;Xie L;Li L;He B;Wu Y;Gu Z
通讯作者:
Gu Z
影响因子:
--
作者:
Hirai, Masahiko;Hiramatsu, Yoshie;Seno, Masaharu
通讯作者:
Seno, Masaharu
DOI:
10.1006/bbrc.1996.5898
发表时间:
1997-01-13
影响因子:
3.1
作者:
Muller, I;Jenner, A;Halliwell, B
通讯作者:
Halliwell, B
DOI:
10.2147/cpaa.s42689
发表时间:
2013
期刊:
Clinical pharmacology : advances and applications
影响因子:
--
作者:
Portell CA;Wenzell CM;Advani AS
通讯作者:
Advani AS
影响因子:
3.7
作者:
Yoshida M;Takimoto R;Murase K;Sato Y;Hirakawa M;Tamura F;Sato T;Iyama S;Osuga T;Miyanishi K;Takada K;Hayashi T;Kobune M;Kato J
通讯作者:
Kato J