Cheng Y, Lotan R
Department of Tumor Biology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.
J Biol Chem. 1998 Dec 25;273(52):35008-15. doi: 10.1074/jbc.273.52.35008.
The effects of retinoids such as all-trans-retinoic acid (ATRA) on cell growth, differentiation, and apoptosis are thought to be mediated by nuclear retinoid receptors, which are involved in ligand-dependent transcriptional activation of target genes. Using differential display, we identified the cDNA of a novel gene, designated retinoic acid-inducible gene 1 (RAIG1), which was induced by ATRA in the squamous carcinoma cell line UMSCC-22B. Two RAIG1 transcripts of 2.4 and 6.8 kilobase pairs, respectively, have the same ORF that encodes a 357-amino acid polypeptide. RAIG1 mRNA is expressed at high level in fetal and adult lung tissues. Induction of RAIG1 expression by ATRA is rapid (within 2 h) and dose-dependent in the range between 1 nM to 1 microM. The constitutive RAIG1 mRNA levels, which were low in three of five head and neck and four of six lung cancer cell lines, increased after ATRA treatment in most cell lines. The deduced RAIG1 protein sequence contains seven transmembrane domains, characteristic of G protein-coupled receptors. A fusion protein of RAIG1 and the green fluorescent protein was localized in the cell surface membrane and perinuclear vesicles in transiently transfected cells. RAIG1 was mapped to chromosome 12p12. 3-p13. Our results provide novel evidence for a possible interaction between retinoid and G protein signaling pathways.
诸如全反式维甲酸(ATRA)等维甲酸类物质对细胞生长、分化及凋亡的影响被认为是由核维甲酸受体介导的,这些受体参与靶基因的配体依赖性转录激活。利用差异显示技术,我们鉴定出一个新基因的cDNA,命名为维甲酸诱导基因1(RAIG1),它在鳞状癌细胞系UMSCC - 22B中被ATRA诱导。分别为2.4和6.8千碱基对的两种RAIG1转录本具有相同的开放阅读框,编码一个357个氨基酸的多肽。RAIG1 mRNA在胎儿和成人肺组织中高水平表达。ATRA对RAIG1表达的诱导迅速(2小时内),且在1 nM至1 microM范围内呈剂量依赖性。在五个头颈癌细胞系中的三个以及六个肺癌细胞系中的四个中,组成型RAIG1 mRNA水平较低,而在大多数细胞系中,经ATRA处理后其水平升高。推导的RAIG1蛋白序列包含七个跨膜结构域,这是G蛋白偶联受体的特征。RAIG1与绿色荧光蛋白的融合蛋白在瞬时转染细胞中定位于细胞表面膜和核周小泡。RAIG1被定位于12号染色体的p12.3 - p13区域。我们的结果为维甲酸与G蛋白信号通路之间可能的相互作用提供了新的证据。