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肠道富集型Krüppel样因子基因在多发性肠道肿瘤小鼠的肠道腺瘤以及家族性腺瘤性息肉病患者的结肠腺瘤中表达降低。

Decreased expression of the gut-enriched Krüppel-like factor gene in intestinal adenomas of multiple intestinal neoplasia mice and in colonic adenomas of familial adenomatous polyposis patients.

作者信息

Dang D T, Bachman K E, Mahatan C S, Dang L H, Giardiello F M, Yang V W

机构信息

Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

出版信息

FEBS Lett. 2000 Jul 7;476(3):203-7. doi: 10.1016/s0014-5793(00)01727-0.

Abstract

Gut-enriched Krüppel-like factor (GKLF) is a zinc finger-containing transcription factor, the expression of which is associated with growth arrest. We compared Gklf expression in intestinal and colonic adenomas to normal mucosa in multiple intestinal neoplasia (Min) mice and familial adenomatous polyposis (FAP) patients, respectively, using semi-quantitative RT-PCR. In Min mice, the level of Gklf transcript is highest in normal-appearing intestinal tissues and decreases as the size of the adenoma increases. In FAP patients, the level of GKLF transcript is lower in adenomas compared to paired normal-appearing mucosa from the same patient or normal colonic mucosa from control individuals without FAP. The possibility of DNA methylation as a cause for the decreased expression of Gklf in adenomas of Min mice was investigated by methylation-specific PCR. Results indicate that the Gklf gene is not methylated in either normal or tumorous tissues. The findings of our study are therefore consistent with the potential role of GKLF as a negative growth regulator of gut epithelial cells.

摘要

肠道富集型锌指蛋白(GKLF)是一种含锌指结构的转录因子,其表达与生长停滞相关。我们分别使用半定量逆转录聚合酶链反应(RT-PCR),比较了肠道和结肠腺瘤中Gklf的表达与多肠肿瘤(Min)小鼠及家族性腺瘤性息肉病(FAP)患者正常黏膜中的表达情况。在Min小鼠中,Gklf转录本水平在外观正常的肠道组织中最高,并随着腺瘤大小的增加而降低。在FAP患者中,与同一患者配对的外观正常黏膜或无FAP的对照个体的正常结肠黏膜相比,腺瘤中GKLF转录本水平较低。通过甲基化特异性PCR研究了DNA甲基化作为Min小鼠腺瘤中Gklf表达降低原因的可能性。结果表明,Gklf基因在正常组织或肿瘤组织中均未发生甲基化。因此,我们的研究结果与GKLF作为肠道上皮细胞负生长调节因子的潜在作用一致。

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