Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY, USA.
Department of Cancer Genetics, Roswell Park Cancer Institute, Buffalo, NY, USA.
Cell Rep. 2017 Sep 19;20(12):2820-2832. doi: 10.1016/j.celrep.2017.08.057.
Lineage-specific regulation of tumor progression by the same transcription factor is understudied. We find that levels of the FOXQ1 transcription factor, an oncogene in carcinomas, are decreased during melanoma progression. Moreover, in contrast to carcinomas, FOXQ1 suppresses epithelial-to-mesenchymal transition, invasion, and metastasis in melanoma cells. We find that these lineage-specific functions of FOXQ1 largely depend on its ability to activate (in carcinomas) or repress (in melanoma) transcription of the N-cadherin gene (CDH2). We demonstrate that FOXQ1 interacts with nuclear β-catenin and TLE proteins, and the β-catenin/TLE ratio, which is higher in carcinoma than melanoma cells, determines the effect of FOXQ1 on CDH2 transcription. Accordingly, other FOXQ1-dependent phenotypes can be manipulated by altering nuclear β-catenin or TLE proteins levels. Our data identify FOXQ1 as a melanoma suppressor and establish a mechanism underlying its inverse lineage-specific transcriptional regulation of transformed phenotypes.
同一种转录因子对肿瘤进展的谱系特异性调控研究较少。我们发现,癌基因 FOXQ1 转录因子的水平在黑色素瘤进展过程中降低。此外,与癌不同,FOXQ1 抑制黑色素瘤细胞中的上皮-间充质转化、侵袭和转移。我们发现 FOXQ1 的这些谱系特异性功能在很大程度上取决于其激活(在癌中)或抑制(在黑色素瘤中)N-钙黏蛋白基因(CDH2)转录的能力。我们证明 FOXQ1 与核 β-连环蛋白和 TLE 蛋白相互作用,β-连环蛋白/TLE 比值在癌中高于黑色素瘤细胞,决定了 FOXQ1 对 CDH2 转录的影响。因此,通过改变核 β-连环蛋白或 TLE 蛋白的水平可以操纵其他依赖 FOXQ1 的表型。我们的数据将 FOXQ1 鉴定为黑色素瘤的抑制因子,并建立了其对转化表型的反谱系特异性转录调控的机制。