Busulfan inhibits growth of human osteosarcoma through miR-200 family microRNAs in vitro and in vivo.
Busulfan inhibits growth of human osteosarcoma through miR-200 family microRNAs in vitro and in vivo.
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DOI:
10.1111/cas.12436
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发表时间:
2014-07
期刊:
影响因子:
5.7
通讯作者:
Xu H
中科院分区:
文献类型:
--
作者:
Mei Q;Li F;Quan H;Liu Y;Xu H
Osteosarcoma typically arises in tissues of mesenchymal origin, and is the most malignant bone tumor characterized by high local aggressiveness, with poor therapeutic outcome. Busulfan has been widely used to treat CML. So far, there are no reports on the therapeutic effect of busulfan on osteosarcoma. Here, we showed that busulfan dose-dependently reduced the cell viability and proliferation, and induced cell apoptosis, senescence, and reactive oxygen species levels in two osteosarcoma cell lines. Moreover, a series of loss-of-function and gain-of-function experiments further indicated that busulfan may have its anti-osteosarcoma effect by upregulating the microRNA-200 (miR-200) family which subsequently downregulated its target genes ZEB1 and ZEB2. Furthermore, treatment with busulfan potentially inhibited the growth of implanted osteosarcoma in nude mice. Taken together, our data suggest that busulfan may have an anti-osteosarcoma effect through downregulating ZEB1 and ZEB2 through activating the miR-200 family, highlighting a possibility of using busulfan as a novel therapy for osteosarcoma.
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影响因子:
11.2
作者:
Jones KB;Salah Z;Del Mare S;Galasso M;Gaudio E;Nuovo GJ;Lovat F;LeBlanc K;Palatini J;Randall RL;Volinia S;Stein GS;Croce CM;Lian JB;Aqeilan RI
通讯作者:
Aqeilan RI
影响因子:
3.1
作者:
Liang, Wenqing;Gao, Bo;Fu, Qingge
通讯作者:
Fu, Qingge
DOI:
10.1007/978-1-60761-411-1_4
发表时间:
2010-01-01
期刊:
ADVANCED PROTOCOLS IN OXIDATIVE STRESS II
影响因子:
--
作者:
Eruslanov, Evgeniy;Kusmartsev, Sergei
通讯作者:
Kusmartsev, Sergei
影响因子:
3.6
作者:
Goldman, John M.
通讯作者:
Goldman, John M.
DOI:
10.1182/asheducation-2008.1.418
发表时间:
2008-01-01
期刊:
Hematology. American Society of Hematology. Education Program
影响因子:
--
作者:
Deininger, Michael W
通讯作者:
Deininger, Michael W