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首页> 外文期刊>Pancreatology: official journal of the International Association of Pancreatology (IAP) ... [et al.] >Effect of FHIT gene replacement on growth, cell cycle and apoptosis in pancreatic cancer cells.
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Effect of FHIT gene replacement on growth, cell cycle and apoptosis in pancreatic cancer cells.

机译：FHIT基因替换对胰腺癌细胞生长，细胞周期和凋亡的影响。

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摘要

The human FHIT gene is altered or lost in many cancers and FHIT has been shown to be a tumor suppressor. However, the mechanism of tumor suppression by the FHIT gene remains unclear. FHIT expression is lost in primary pancreatic cancer and human pancreatic cancer cell lines. To gain insight into the function of FHIT gene, we replaced the FHIT gene in a FHIT-null pancreatic cancer cell line, and established stable fhit-expressing clones. Expression of the exogenous fhit was at similar levels as in other cultured cell lines and fhit protein was found predominantly associated with perinuclear area. fhit replacement resulted in reduced cell proliferation in transfected Panc-1 cells. Cell cycle distribution analysis indicated increased accumulation of G(0)/G(1) phase cells in transfected clones indicating a retardation of cell cycle progression. We observed specific up-regulation of cdc2 and cyclin D3 upon fhit replacement. Furthermore, Bcl-2 family members Bad, Bak, and Bcl-xS protein levels were increasedin FHIT transfected clones when compared with Panc-1 cells. Multiplex RT-PCR of apoptosis pathway related genes revealed that Bcl-2 is absent and Bcl- xS message increases in FHIT transfected clones. Our data suggested that exogenous expression of FHIT in Panc-1 cells affects genes regulating cell cycle arrest and apoptosis, and these molecular changes may contribute to the tumor suppressor activity of the FHIT gene.
机译：人类FHIT基因在许多癌症中都会发生改变或丢失，并且已证明FHIT是一种肿瘤抑制因子。但是，FHIT基因抑制肿瘤的机制仍不清楚。 FHIT表达在原发性胰腺癌和人类胰腺癌细胞系中丢失。为了深入了解FHIT基因的功能，我们在FHIT空胰腺癌细胞系中替换了FHIT基因，并建立了稳定的表达表达的克隆。外源斑点的表达与其他培养的细胞系中的表达相似，并且斑点蛋白主要与核周区域有关。 Fhit替换导致转染的Panc-1细胞中的细胞增殖减少。细胞周期分布分析表明，G（0）/ G（1）相细胞在转染克隆中的积累增加，表明细胞周期进程的延迟。我们观察到敲击替换后cdc2和cyclin D3的特异性上调。此外，与Panc-1细胞相比，FHIT转染的克隆中Bcl-2家族成员Bad，Bak和Bcl-xS蛋白水平升高。凋亡通路相关基因的多重RT-PCR显示在FHIT转染的克隆中不存在Bcl-2，Bcl-xS信息增加。我们的数据表明Panc-1细胞中FHIT的外源表达影响调节细胞周期停滞和凋亡的基因，这些分子的变化可能有助于FHIT基因的抑癌活性。

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