Romero-Ramirez Lorenzo, Cao Hongbin, Nelson Daniel, Hammond Ester, Lee Ann-Hwee, Yoshida Hiderou, Mori Kazutoshi, Glimcher Laurie H, Denko Nicholas C, Giaccia Amato J, Le Quynh-Thu, Koong Albert C
Department of Radiation Oncology, Stanford University, Stanford, California 94305-5152, USA.
Cancer Res. 2004 Sep 1;64(17):5943-7. doi: 10.1158/0008-5472.CAN-04-1606.
Hypoxia within solid tumors is a major determinant of outcome after anticancer therapy. Analysis of gene expression changes during hypoxia indicated that unfolded protein response genes were one of the most robustly induced groups of genes. In this study, we investigated the hypoxic regulation of X-box binding protein (XBP1), a major transcriptional regulator of the unfolded protein response. Hypoxia induced XBP1 at the transcriptional level and activated splicing of its mRNA, resulting in increased levels of activated XBP1 protein. After exposure to hypoxia, apoptosis increased and clonogenic survival decreased in XBP1-deficient cells. Loss of XBP1 severely inhibited tumor growth due to a reduced capacity for these transplanted tumor cells to survive in a hypoxic microenvironment. Taken together, these studies directly implicate XBP1 as an essential survival factor for hypoxic stress and tumor growth.
实体瘤内的缺氧是抗癌治疗后预后的主要决定因素。对缺氧过程中基因表达变化的分析表明,未折叠蛋白反应基因是诱导最强烈的基因群体之一。在本研究中,我们研究了未折叠蛋白反应的主要转录调节因子X盒结合蛋白(XBP1)的缺氧调节。缺氧在转录水平诱导XBP1,并激活其mRNA的剪接,导致活化的XBP1蛋白水平增加。暴露于缺氧后,XBP1缺陷细胞中的凋亡增加,克隆形成存活率降低。由于这些移植的肿瘤细胞在缺氧微环境中存活的能力降低,XBP1的缺失严重抑制了肿瘤生长。综上所述,这些研究直接表明XBP1是缺氧应激和肿瘤生长的必需生存因子。