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首页> 外文期刊>Oncogene >The transcriptional factor YY1 upregulates the novel invasion suppressor HLJ1 expression and inhibits cancer cell invasion
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The transcriptional factor YY1 upregulates the novel invasion suppressor HLJ1 expression and inhibits cancer cell invasion

机译：转录因子YY1上调新型侵袭抑制因子HLJ1的表达并抑制癌细胞的侵袭

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By using microarray and an invasion/metastasis lung cell line model, we identified the DnaJ-like heat shock protein 40, HLJ1, and found that the expression of HLJ1 correlates negatively with cancer cell invasion ability. Overexpression of HLJ1 can suppress cancer cell invasion in vitro. We further characterize the putative promoter region and investigate the transcriptional regulations of human HLJ1. A serial deletion of the 1.2kb at the 5'-flanking region of the human HLJ1 gene was subcloned into a vector containing reporter gene and transfected into human lung adenocarcinoma cell line CL1-0, followed by luciferase activity assay. The results indicated that the region from –232 to +176 could drive the basal transcriptional activity of the HLJ1 gene. Sequence analysis of the HLJ1 gene promoter region showed absence of a TATA box, but identified an inverted CCAAT box and four YY1 transcriptional factor-binding sites, which may be important in the regulation of HLJ1 expression. Co-transfection of the YY1 and HLJ1 basal promoter regions, site-directed mutagenesis, and electrophoretic mobility shift assay confirmed that YY1 could upregulate HLJ1 basal promoter activity. Furthermore, we also demonstrated that overexpression of YY1 in CL1-0 cells can increase HLJ1 expression and reduce cell invasive capability. The reduction of cancer cell invasive ability is, at least in part, through upregulation of E-cadherin expression. The increase in HLJ1 and E-cadherin expression, as well as the suppression of invasion ability, can be reversed specifically by HLJ1 siRNA.
机译：通过使用芯片和侵袭/转移肺细胞系模型，我们确定了DnaJ样热休克蛋白40，HLJ1，并发现HLJ1的表达与癌细胞侵袭能力负相关。 HLJ1的过表达可以在体外抑制癌细胞的侵袭。我们进一步表征推定的启动子区域，并调查人类HLJ1的转录调控。将人HLJ1基因的5'侧翼区域的1.2kb的序列缺失亚克隆到含有报告基因的载体中，并转染到人肺腺癌细胞系CL1-0中，然后进行荧光素酶活性测定。结果表明，从–232到+176的区域可以驱动HLJ1基因的基础转录活性。 HLJ1基因启动子区的序列分析显示没有TATA框，但鉴定出一个倒置的CCAAT框和四个YY1转录因子结合位点，这可能在调节HLJ1表达中很重要。 YY1和HLJ1基础启动子区域的共转染，定点诱变和电泳迁移率变动分析证实YY1可以上调HLJ1基础启动子活性。此外，我们还证明了CL1-0细胞中YY1的过表达可以增加HLJ1表达并降低细胞侵袭能力。癌细胞侵袭能力的降低至少部分是通过上调E-钙粘蛋白表达来实现的。 HLJ1 siRNA可特异性逆转HLJ1和E-钙黏着蛋白表达的增加以及对侵袭能力的抑制。

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