Ha Bin, Lee Eun Byul, Cui Jun, Kim Yosup, Jang Ho Hee
Department of Molecular Medicine, Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon 406-799, Republic of Korea.
Department of Molecular Medicine, Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon 406-799, Republic of Korea; Gachon Medical Research Institute, Gil Medical Center, Gachon University, Incheon, Republic of Korea.
Biochem Biophys Res Commun. 2015 Mar 6;458(2):347-51. doi: 10.1016/j.bbrc.2015.01.114. Epub 2015 Jan 30.
The Y-box binding protein-1 (YB-1) is a transcription/translation regulatory protein, and the expression thereof is associated with cancer aggressiveness. In the present study, we explored the regulatory effects of YB-1 during the transforming growth factor-β1 (TGF-β1)-induced epithelial-to-mesenchymal transition (EMT) in lung adenocarcinoma cells. Downregulation of YB-1 increased E-cadherin promoter activity, and upregulation of YB-1 decreased promoter activity, suggesting that the YB-1 level may be correlated with the EMT. TGF-β1 induced YB-1 expression, and TGF-β1 translocated cytosolic YB-1 into the nucleus. YB-1 overexpression promoted TGF-β1-induced downregulation of epithelial markers, upregulation of mesenchymal markers, and cell migration. Moreover, YB-1 overexpression enhanced the expression of E-cadherin transcriptional repressors via TGF-β1-induced Akt activation. Our findings afford new insights into the role played by YB-1 in the TGF-β1 signaling pathway.
Y盒结合蛋白1（YB-1）是一种转录/翻译调节蛋白，其表达与癌症侵袭性相关。在本研究中，我们探讨了YB-1在转化生长因子-β1（TGF-β1）诱导的肺腺癌细胞上皮-间质转化（EMT）过程中的调节作用。YB-1的下调增加了E-钙黏蛋白启动子活性，而YB-1的上调则降低了启动子活性，这表明YB-1水平可能与EMT相关。TGF-β1诱导YB-1表达，并使胞质中的YB-1转位至细胞核。YB-1过表达促进了TGF-β1诱导的上皮标志物下调、间质标志物上调以及细胞迁移。此外，YB-1过表达通过TGF-β1诱导的Akt激活增强了E-钙黏蛋白转录抑制因子的表达。我们的研究结果为YB-1在TGF-β1信号通路中所起的作用提供了新的见解。
