Genetics Unit, Hospital Universitario Marqués de Valdecilla and Instituto de Investigación Marqués de Valdecilla (IDIVAL), Avda. Valdecilla s/n, 39008, Santander, Spain.
Neurosurgery Service, Hospital Universitario Marqués de Valdecilla and Instituto de Investigación Marqués de Valdecilla (IDIVAL), 39008, Santander, Spain.
Sci Rep. 2021 Aug 10;11(1):16196. doi: 10.1038/s41598-021-95753-6.
We have previously shown that the transmembrane protein ODZ1 serves for glioblastoma (GBM) cells to invade the surrounding tissue through activation of RhoA/ROCK pathway. However, the transcriptional machinery used by GBM cells to regulate the expression of ODZ1 is unknown. Here we show that interaction with tumor microenvironment elements, mainly activated monocytes through IL-6 secretion, and the extracellular matrix protein fibronectin, induces the Stat3 transcriptional pathway and upregulates ODZ1 which results in GBM cell migration. This signaling route is abrogated by blocking the IL-6 receptor, inhibiting Jak kinases or knocking down Stat3. Furthermore, we have identified a Stat3 responsive element in the ODZ1 gene promoter, about 1 kb from the transcription start site. Luciferase-reporter assays confirmed that the promoter responds to the presence of monocytic cells and this activation is greatly reduced when the Stat3 site is mutated or following treatment with a neutralizing anti-IL-6 receptor antibody or transfecting GBM cells with a dominant negative variant of Stat3. Overall, we show that monocyte-secreted IL-6 and the extracellular matrix protein fibronectin activate the axis Stat3-ODZ1 and promote migration of GBM cells. This is the first described transcriptional mechanism used by tumor cells to promote the expression of the invasion factor ODZ1.
我们之前已经表明,跨膜蛋白 ODZ1 通过激活 RhoA/ROCK 通路,使神经胶质瘤(GBM)细胞能够侵袭周围组织。然而,GBM 细胞用来调节 ODZ1 表达的转录机制尚不清楚。在这里,我们表明与肿瘤微环境元素的相互作用,主要是通过 IL-6 分泌激活的单核细胞和细胞外基质蛋白纤维连接蛋白,诱导 Stat3 转录途径并上调 ODZ1,从而导致 GBM 细胞迁移。通过阻断 IL-6 受体、抑制 Jak 激酶或敲低 Stat3,可以阻断这种信号通路。此外,我们已经在 ODZ1 基因启动子中鉴定到一个 Stat3 反应元件,距离转录起始位点约 1kb。荧光素酶报告基因检测证实,启动子对单核细胞的存在有反应,而当 Stat3 位点发生突变或用中和抗 IL-6 受体抗体处理或用显性负变异体转染 GBM 细胞时,这种激活大大减少。总的来说,我们表明单核细胞分泌的 IL-6 和细胞外基质蛋白纤维连接蛋白激活了 Stat3-ODZ1 轴,并促进了 GBM 细胞的迁移。这是第一个描述肿瘤细胞用来促进侵袭因子 ODZ1 表达的转录机制。