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结肠癌细胞中过氧化物酶体增殖物激活受体γ的靶基因。

Target genes of peroxisome proliferator-activated receptor gamma in colorectal cancer cells.

作者信息

Gupta R A, Brockman J A, Sarraf P, Willson T M, DuBois R N

机构信息

Departments of Medicine and Cell Biology, Vanderbilt University Medical Center and Veterans Affairs Medical Center, Nashville, Tennessee 37232, USA.

出版信息

J Biol Chem. 2001 Aug 10;276(32):29681-7. doi: 10.1074/jbc.M103779200. Epub 2001 Jun 7.

Abstract

Activation of the nuclear hormone peroxisome proliferator-activated receptor gamma (PPARgamma) inhibits cell growth and promotes differentiation in a broad spectrum of epithelial derived tumor cell lines. Here we utilized microarray technology to identify PPARgamma gene targets in intestinal epithelial cells. For each gene, the induction or repression was seen with two structurally distinct PPARgamma agonists, and the change in expression could be blocked by co-treatment with a specific PPARgamma antagonist. A majority of the genes could be regulated independently by a retinoid X receptor specific agonist. Genes implicated in lipid transport or storage (adipophilin and liver fatty acid-binding protein) were also activated by agonists of PPAR subtypes alpha and/or delta. In contrast, PPARgamma-selective targets included genes linked to growth regulatory pathways (regenerating gene IA), colon epithelial cell maturation (GOB-4 and keratin 20), and immune modulation (neutrophil-gelatinase-associated lipocalin). Additionally, three different genes of the carcinoembryonic antigen family were induced by PPARgamma. Cultured cells treated with PPARgamma ligands demonstrated an increase in Ca(2+)-independent, carcinoembryonic antigen-dependent homotypic aggregation, suggesting a potential role for PPARgamma in regulating intercellular adhesion. Collectively, these results will help define the mechanisms by which PPARgamma regulates intestinal epithelial cell biology.

摘要

核激素过氧化物酶体增殖物激活受体γ(PPARγ)的激活可抑制多种上皮来源肿瘤细胞系的细胞生长并促进其分化。在此,我们利用微阵列技术来鉴定肠上皮细胞中的PPARγ基因靶点。对于每个基因,两种结构不同的PPARγ激动剂均可诱导或抑制其表达,且与特异性PPARγ拮抗剂共同处理可阻断表达变化。大多数基因可由视黄酸X受体特异性激动剂独立调节。参与脂质转运或储存的基因(脂联素和肝脏脂肪酸结合蛋白)也可被PPARα和/或δ亚型的激动剂激活。相比之下,PPARγ选择性靶点包括与生长调节途径相关的基因(再生基因IA)、结肠上皮细胞成熟相关基因(GOB-4和角蛋白20)以及免疫调节相关基因(中性粒细胞明胶酶相关脂质运载蛋白)。此外,癌胚抗原家族的三个不同基因也可被PPARγ诱导。用PPARγ配体处理的培养细胞显示出非钙依赖性、癌胚抗原依赖性同型聚集增加,这表明PPARγ在调节细胞间黏附中可能发挥作用。总体而言,这些结果将有助于明确PPARγ调节肠上皮细胞生物学的机制。

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