Roles of HES1 and DEC2, newly identified transcriptional targets of GLI1, in pancreatic carcinogenesis.

新发现的 GLI1 转录靶标 HES1 和 DEC2 在胰腺癌发生中的作用。

• 批准号: 21790370
• 负责人: INAGUMA Shingo
• 金额: $ 1.83万
• 依托单位: Aichi Medical University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2009
• 资助国家: 日本
• 起止时间: 2009 至 2010
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21790370/
• 关键词: 分子病理; 膵臓癌; シグナル伝達; ヘッジホッグ; 転写因子; GLI1

We identified DEC2 as one of the direct transcriptional targets of GLI1, a downstream transcription factor of Hedgehog signaling pathway, via CACCC-box-like elements localized between -1126 and -1117 in the DEC2 promoter. We also showed that one of the mismatch repair gene MLH1 was down-regulated by GLI1-induced DEC2. We propose the possibility that Shh-GLI1-DEC2 pathway represses MLH1 expression and could enhance gene alteration and genomic instability in pancreatic carcinogenesis.

我们通过位于DEC 2启动子-1126和-1117之间的CACCC盒样元件鉴定DEC 2是Hedgehog信号通路下游转录因子GLI 1的直接转录靶点之一。我们还发现，错配修复基因MLH 1下调GLI 1诱导的DEC 2。我们提出Shh-GLI 1-DEC 2通路抑制MLH 1表达的可能性，并可能在胰腺癌发生中增强基因改变和基因组不稳定性。

项目成果

GLI1 induces the expression of bHLH type of transcriptional repressor DEC2 in pancreatic cancer cells.

GLI1 诱导胰腺癌细胞中 bHLH 型转录抑制因子 DEC2 的表达。

• 发表时间: 2010
• 作者: Inaguma S.;et al.
• 通讯作者: et al.

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