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胆碱缺乏 L-氨基酸定义饮食诱导大鼠肝癌发生过程中溶血磷脂酸受体基因的独特 DNA 甲基化模式。

Distinct DNA methylation patterns of lysophosphatidic acid receptor genes during rat hepatocarcinogenesis induced by a choline-deficient L-amino acid-defined diet.

机构信息

Division of Cancer Biology and Bioinformatics, Department of Life Science, Faculty of Science and Engineering, Kinki University, 3-4-1, Kowakae, Higashiosaka, Osaka 577-8502, Japan.

出版信息

Arch Toxicol. 2011 Oct;85(10):1303-10. doi: 10.1007/s00204-011-0656-7. Epub 2011 Feb 3.

Abstract

Altered expressions of lysophosphatidic acid (LPA) receptor genes have been reported in tumor cells of human and rats. Recently, we detected the frequent mutations of LPA receptor-1 (LPA1) gene in rat hepatocellular carcinomas (HCCs) induced by a choline-deficient L-amino acid-defined (CDAA) diet. In this study, the DNA methylation patterns of LPA receptor genes and their expression levels during rat hepatocarcinogenesis induced by the CDAA diet were investigated. Six-week-old F344 male rats were continuously fed with the CDAA diet, and animals were then killed at 7 days and 2, 12, 20, and 75 weeks, respectively. Genomic DNAs were extracted from livers and HCCs for the assessment of methylation status by bisulfite sequencing, comparing to normal livers. The livers of rats fed the CDAA diet were unmethylated in LPA1 and LPA2 genes as well as normal livers. In LPA3 gene, although normal livers were unmethylated, the livers at 7 days and 2 and 12 weeks weakly or moderately methylated and those at 20 weeks markedly methylated. Moreover, 4 HCCs were completely methylated in LPA3 gene. Expression levels of LPA receptor genes in the livers of rats fed the CDAA diet and HCCs were correlating with DNA methylation status. These results indicate that DNA methylation status of the LPA3 gene was disturbed in the livers of rats fed the CDAA diet and established HCCs, suggesting that alterations of the LPA receptor genes might be involved during rat hepatocarcinogenesis induced by the CDAA diet.

摘要

已报道在人类和大鼠的肿瘤细胞中存在溶血磷脂酸(LPA)受体基因表达的改变。最近,我们在胆碱缺乏 L-氨基酸定义(CDAA)饮食诱导的大鼠肝癌(HCC)中检测到 LPA 受体-1(LPA1)基因的频繁突变。在这项研究中,我们研究了在 CDAA 饮食诱导的大鼠肝癌发生过程中 LPA 受体基因的 DNA 甲基化模式及其表达水平。6 周龄 F344 雄性大鼠连续喂食 CDAA 饮食,然后分别在第 7 天、2、12、20 和 75 周处死动物。从肝脏和 HCC 中提取基因组 DNA,通过亚硫酸氢盐测序评估甲基化状态,与正常肝脏进行比较。喂食 CDAA 饮食的大鼠肝脏中 LPA1 和 LPA2 基因未甲基化,与正常肝脏一样。在 LPA3 基因中,尽管正常肝脏未甲基化,但在第 7 天、2 周和 12 周时,肝脏弱或中度甲基化,在 20 周时明显甲基化。此外,4 个 HCC 在 LPA3 基因中完全甲基化。喂食 CDAA 饮食的大鼠肝脏和 HCC 中 LPA 受体基因的表达水平与 DNA 甲基化状态相关。这些结果表明,喂食 CDAA 饮食的大鼠肝脏和建立的 HCC 中 LPA3 基因的 DNA 甲基化状态受到干扰,提示 LPA 受体基因的改变可能参与了 CDAA 饮食诱导的大鼠肝癌发生过程。

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