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Conditional knockout of brca1/2 and p53 in mouse ovarian surface epithelium: Do they play a role in ovarian carcinogenesis?

机译:小鼠卵巢表面上皮细胞中条件性敲除brca1 / 2和p53:它们是否在卵巢癌发生中起作用?

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摘要

Alterations of genes are known to be critical for the induction of tumorigenesis, but the mechanism of ovarian carcinogenesis is little understood and remains to be elucidated. In this study, we investigated the roles of brca1, brca2 and p53 genes in the development of ovarian cancer using conditional knockout mice generated by a Cre-loxP recombinant system. Following the application of recombinant adenovirus expressing Cre in vitro, the proliferation of ovarian surface epithelium (OSE) was increased. For instance, a significant increase in cell growth was observed in OSE cells in vitro by conditional knockout isolated from the mice bearing concurrent floxed copies of brca1 and brca2/p53. However, the proliferative effect of the ovarian cells was not observed in concurrent brca1/brca2 or p53 knockout mice in vivo, indicating that we could not observe the direct evidence of the involvement of brca1, brca2, and p53 in ovarian carcinogenesis. Since morphological changes including tumor formation were not observed in mice bearing floxed copies of concurrent brca1/brca2 or p53, the inactivation of brca1/2 or p53 is not sufficient for the induction of tumor formation. Taken together, these results suggest that the deficiency of these genes may not be involved directly in the mechanism of ovarian carcinogenesis.
机译:已知基因的改变对于诱导肿瘤发生至关重要,但是卵巢癌发生的机制尚不清楚,尚待阐明。在这项研究中,我们使用Cre-loxP重组系统产生的条件敲除小鼠,调查了brca1,brca2和p53基因在卵巢癌发展中的作用。在应用表达体外Cre的重组腺病毒后,卵巢表面上皮(OSE)的增殖增加。例如,通过有条件的基因敲除,从小鼠身上同时观察到brca1和brca2 / p53连锁拷贝,分离出有条件的敲除,在OSE细胞中观察到细胞生长的显着增加。但是,在并发的brca1 / brca2或p53基因敲除小鼠体内未观察到卵巢细胞的增殖作用,这表明我们无法观察到brca1,brca2和p53参与卵巢癌发生的直接证据。由于在携带并发的brca1 / brca2或p53拷贝的小鼠中未观察到包括肿瘤形成在内的形态学变化,因此brca1 / 2或p53的失活不足以诱导肿瘤形成。综上所述,这些结果表明这些基因的缺乏可能不直接参与卵巢癌的发生机理。

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