兰克尔
细胞凋亡
阿霉素
肿瘤坏死因子α
受体
激活剂(遗传学)
Fas配体
癌症研究
化学
细胞生物学
生物
分子生物学
内分泌学
程序性细胞死亡
生物化学
化疗
遗传学
作者
Ingo Müller,Stefan M. Pfister,Ulrike Grohs,Janine Zweigner,Rupert Handgretinger,D. Niethammer,Gernot Bruchelt
出处
期刊:PubMed
日期:2003-04-15
卷期号:63 (8): 1772-5
被引量:5
摘要
Doxorubicin induces apoptosis in a variety of cells. We investigated the expression and function of various tumor necrosis factor (TNF)alpha-homologues and their receptors. CEM cells did not differentially express any one of the TNFalpha-homologous receptors investigated nor TNF-related apoptosis-inducing ligand or TNF-related weakly apoptosis-inducing ligand (TWEAK) in the presence of doxorubicin. In addition to CD95 ligand, however, receptor activator of nuclear factor kappaB ligand (RANKL) was strongly up-regulated. Doxorubicin-induced apoptosis was greatly suppressed in the presence of either neutralizing antibody or RANK-Fc fusion protein. Moreover, neutralizing RANKL also prevented cytochrome c release from mitochondria. RANKL alone was unable to induce significant levels of apoptosis in CEM cells. However, doxorubicin-induced apoptosis was increased >2-fold when exogenous RANKL was added. Therefore, RANKL is necessary but not sufficient to account for early doxorubicin-induced apoptosis in CEM cells. This finding suggests improved chemotherapeutic efficiency of the anthracyclin against susceptible malignant cells in the presence with RANKL.
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