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首页> 外文期刊>Journal of cellular biochemistry. >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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Hyperthermia inhibits cell proliferation and induces apoptosis: relative signaling status of P53, S100A4, and Notch in heat sensitive and resistant cell lines.

机译:热疗抑制细胞增殖并诱导细胞凋亡:P53,S100A4和Notch在热敏感和耐药细胞系中的相对信号状态。

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摘要

The effects of hyperthermia on the expression of p53, 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 p53, Bax, Bcl-2, Notch, and S100A4 genes. The induction of apoptosis and the inhibition of cell proliferation occurred independently of p53, 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 p53, 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.
机译:在适合于在高温条件下生长的HepG2细胞系和HepG2衍生的HUT细胞系中,研究了热疗对p53,凋亡相关基因Bax和Bcl-2,Notch和S100A4表达的影响。热疗抑制细胞增殖并诱导凋亡。 HepG2和HUT细胞在对生长表面的锚定,增殖和凋亡程度以及p53,Bax,Bcl-2,Notch和S100A4基因的表达方面有所不同。凋亡的诱导和细胞增殖的抑制独立于p53发生,也独立于凋亡家族基因Bax和Bcl-2的参与。我们证明瞬时热休克和热适应之间的信号传导和表型效应的产生途径之间的新颖和明显的区别。在此已经识别了不同的信令模式。 S100A4,其与p53的相互作用和螯合以及Notch的信号传导途径在诱导凋亡方面似乎也有不同的作用,并且在高热信号传导的情况下,两者都可独立于p53激活为替代途径。

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