Department of Cell Signaling, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, 467-8603, Japan.
Department of Cell Signaling, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, 467-8603, Japan.
Biochem Biophys Res Commun. 2024 May 14;708:149789. doi: 10.1016/j.bbrc.2024.149789. Epub 2024 Mar 16.
The tumor suppressor p53 prevents cancer development by regulating dozens of target genes with diverse biological functions. Although numerous p53 target genes have been identified to date, the dynamics and function of the regulatory network centered on p53 have not yet been fully elucidated. We herein identified inhibitor of DNA-binding/differentiation-3 (ID3) as a direct p53 target gene. p53 bound the distal promoter of ID3 and positively regulated its transcription. ID3 expression was significantly decreased in clinical lung cancer tissues, and was closely associated with overall survival outcomes in these patients. Functionally, ID3 deficiency promoted the metastatic ability of lung cancer cells through its effects on the transcriptional regulation of CDH1. Furthermore, the ectopic expression of ID3 in p53-knockdown cells restored E-cadherin expression. Collectively, the present results demonstrate that ID3 plays a tumor-suppressive role as a downstream effector of p53 and impedes lung cancer cell metastasis by regulating E-cadherin expression.
抑癌基因 p53 通过调节数十种具有不同生物学功能的靶基因来预防癌症的发生。尽管迄今为止已经鉴定出许多 p53 靶基因,但以 p53 为中心的调控网络的动态和功能尚未完全阐明。本研究鉴定出 DNA 结合/分化抑制因子 3(ID3)为 p53 的直接靶基因。p53 结合 ID3 的远端启动子并正向调节其转录。ID3 在临床肺癌组织中的表达显著降低,与这些患者的总生存结局密切相关。功能上,ID3 缺失通过对 CDH1 的转录调控促进肺癌细胞的转移能力。此外,在 p53 敲低细胞中外源表达 ID3 恢复了 E-钙粘蛋白的表达。总之,这些结果表明 ID3 作为 p53 的下游效应因子发挥抑癌作用,并通过调节 E-钙粘蛋白的表达来阻碍肺癌细胞的转移。