Doxorubicin-mediated apoptosis in glioma cells requires NFAT3.
Doxorubicin-mediated apoptosis in glioma cells requires NFAT3.
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DOI：
10.1007/s00018-009-0157-5
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发表时间：
2009-12
影响因子：
8
通讯作者：
Rao, Jasti S.
中科院分区：
文献类型：
--
作者：
Gopinath, Sreelatha;Vanamala, Sravan K.;Gujrati, Meena;Klopfenstein, Jeffrey D.;Dinh, Dzung H.;Rao, Jasti S.
活化T细胞核因子(NFAT)是一个转录因子家族，参与多种细胞过程，包括某些癌症。本研究首次研究了NFAT3在阿霉素(DOX)介导的SNB19和U87胶质瘤细胞的凋亡、迁移和侵袭中的作用。这项研究表明，NFAT3的特异性敲除导致了对DOX诱导的凋亡效应的戏剧性抑制，并有利于细胞存活。ShNFAT3(ShNF3)可显著下调肿瘤坏死因子-α及其受体TnFR1、Caspase10、Caspase3和PARP的表达，阻断多柔比星诱导的细胞凋亡。DOX处理导致NFAT3易位到细胞核。同样，shNF3在SNB19和U87细胞中的处理逆转了DOX诱导的细胞迁移和侵袭的抑制，这是通过伤口愈合和基质侵袭分析确定的。综上所述，这些结果表明，NFAT3是诱导DOX介导的胶质瘤细胞凋亡的先决条件。
Nuclear Factor of Activated T cells (NFAT), a family of transcription factors, has been implicated in many cellular processes, including some cancers. For the first time, the present study characterizes the role of NFAT3 in doxorubicin (DOX) mediated apoptosis, migration, and invasion in SNB19 and U87 glioma cells. This study demonstrates specific knockdown of NFAT3 results in a dramatic inhibition of the apoptotic effect, induced by DOX, and favors cell survival. Inhibition of NFAT3 activation by shNFAT3 (shNF3) significantly downregulated TNF-α induction, its receptor TNFR1, caspase 10, caspase 3 and PARP, abrogating DOX-mediated apoptosis in glioma cells. DOX treatment resulted in NFAT3 translocation to the nucleus. Similarly, shNF3 treatment in SNB19 and U87 cells reversed DOX-induced inhibition of cell migration and invasion as determined by wound healing and matrigel invasion assays. Taken together, these results indicate that NFAT3 is a prerequisite for the induction of DOX-mediated apoptosis in glioma cells.
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