Hyperthermia inhibits cell proliferation and induces apoptosis: Relative signaling status of p53, S100A4, and notch in heat sensitive and resistant cell lines

Hyperthermia inhibits cell proliferation and induces apoptosis: Relative signaling status of p53, S100A4, and notch in heat sensitive and resistant cell lines
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DOI:
10.1002/jcb.21401
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发表时间:
2008-01-01
影响因子:
4
通讯作者:
Cajone, Francesco
Cajone, Francesco
中科院分区:
生物学2区
文献类型:
--
作者:
Basile, Antonio;Biziato, Daniela;Cajone, Francesco

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已经在HepG 2细胞系和源自HepG 2的HUT细胞系中研究了高温对1353、凋亡相关基因Bax和Bcl-2、Notch和S100 A4的表达的影响,所述细胞系适于在高温条件下生长。热疗抑制细胞增殖并诱导细胞凋亡。HepG 2和HUT细胞在生长表面的贴壁、增殖和凋亡程度以及1353、Bax、Bcl-2、Notch和S100 A4基因的表达方面存在差异。细胞凋亡的诱导和细胞增殖的抑制独立于1353,也独立于凋亡家族基因Bax和Bcl-2的参与。我们证明了短暂热休克和热适应之间在信号传导途径和体外表型效应产生方面的新的和显着的差异。这里已经识别出不同的信号模式。通过S100 A4的信号传导途径,通过其与1353的相互作用和隔离,以及通过Notch的信号传导途径在诱导细胞凋亡中似乎也是不同的操作,并且两者似乎在不依赖于p53的高热信号传导的背景下作为替代途径被激活。
The effects of hyperthermia on the expression of 1353, the apoptosis-associated genes Bax and Bcl-2, Notch and S100A4 have been studied in the HepG2 cell line and the HUT cell line derived from HepG2, adapted for growth in hyperthermic conditions. Hyperthermia inhibits cell proliferation and induces apoptosis. HepG2 and HUT cells differed in respect of anchorage to growth surface, degree of proliferation and apoptosis and expression of 1353, Bax, Bcl-2, Notch, and S100A4 genes. The induction of apoptosis and the inhibition of cell proliferation occurred independently of 1353, and independently also of involvement of the apoptosis family genes Bax and Bcl-2. We demonstrate novel and marked differences between transient heat shock and heat adaptation in respect of pathways of signaling and generation of phenotypic effects in vitro. Different signaling patterns have been identified here. Pathways of signaling by S100A4, by its interaction with and sequestration of 1353, and by Notch also seem differentially operational in the induction of apoptosis, and both appear to be activated as alternative pathways in the context of hyperthermia signaling independently of p53.