背景：胶质母细胞瘤（GBM）是一种侵袭性脑肿瘤。整合素与GBM的恶性肿瘤有关。最近的研究表明，整合素α3（ITGA3）通过调节转录因子POU3F2促进乳腺癌细胞的侵袭。然而,这是否也发生在GBM仍然未知。
方法：因此，我们探讨了GBM中ITGA3和POU3F2的关系。我们测定了GBM组织中ITGA3和POU3F2的表达。我们产生了ITGA3敲低和POU3F2敲低GBMU87MG细胞，移民和入侵，测量干性标志物和上皮间质转化（EMT）标志物的表达。我们将ITGA3敲低和POU3F2敲低GBMU87MG细胞移植到小鼠体内。用抗ITGA3抗体处理小鼠。肿瘤的大小,测量了干性标志物和上皮-间质转化(EMT)标志物的表达。
结果：ITGA3和POU3F2在GBM组织中均上调。敲低ITGA3导致POU3F2的表达降低。敲低ITGA3和POU3F2抑制U87MG细胞增殖,移民和入侵，抑制干性标志物的表达并阻止上皮-间质转化。移植ITGA3敲低和POU3F2敲低U87MG细胞减小肿瘤年夜小。
结论：抗ITGA3抗体治疗可减小肿瘤大小。ITGA3通过POU3F2调节胶质母细胞瘤的干性和侵袭。
BACKGROUND: Glioblastoma (GBM) is an aggressive brain tumor. Integrins have been implicated in the malignancy of GBM. A recent study demonstrated that integrin α3 (ITGA3) promoted the invasion of breast cancer cells by regulating transcriptional factor POU3F2. However, whether this also happened in GBM remained unknown.
METHODS: Therefore, we explored the relationship between ITGA3 and POU3F2 in GBM. We measured the expression of ITGA3 and POU3F2 in GBM tissues. We generated ITGA3 knockdown and POU3F2 knockdown GBM U87MG cells and the proliferation, migration and invasion, the expression of stemness markers and epithelial to mesenchymal transition (EMT) markers were measured. We transplanted ITGA3 knockdown and POU3F2 knockdown GBM U87MG cells into mice. The mice were treated with anti-ITGA3 antibody. The tumor sizes, the expression of stemness markers and epithelial-to-mesenchymal transition (EMT) markers were measured.
RESULTS: Both ITGA3 and POU3F2 were upregulated in GBM tissues. Knocking down ITGA3 resulted in reduced expression of POU3F2. Knocking down ITGA3 and POU3F2 suppressed U87MG cells proliferation, migration and invasion, inhibited the expression of stemness markers and prevented epithelial- to-mesenchymal transition. The transplantation of ITGA3 knockdown and POU3F2 knockdown U87MG cells decreased tumor size.
CONCLUSIONS: Anti-ITGA3 antibody treatment reduced the tumor size. ITGA3 regulates stemness and invasion of glioblastoma through POU3F2.
