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首页> 外文期刊>OncoTargets and therapy >Novel role of granulocyte-macrophage colony-stimulating factor: antitumor effects through inhibition of epithelial-to-mesenchymal transition in esophageal cancer
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Novel role of granulocyte-macrophage colony-stimulating factor: antitumor effects through inhibition of epithelial-to-mesenchymal transition in esophageal cancer

机译:粒细胞巨噬细胞集落刺激因子的新作用:通过抑制食管癌中上皮向间充质转化的抗肿瘤作用

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Purpose: Recent studies demonstrate the possible antitumor effects of granulocyte-macrophage colony-stimulating factor (GM-CSF); however, the exact mechanism is still unclear. The aim of our study was to analyze the effects of GM-CSF on multiple biological functions of human esophageal cancer (EC) cell lines and to explore the potential mechanism of its antitumor effects. Materials and methods: Eca109/9706 human EC cells were examined. Cell proliferation, apoptosis, and migration were analyzed using cell proliferation assay, flow cytometry, and transwell assay, respectively. The expression of signaling molecules were examined by reverse transcription polymerase chain reaction and Western blot. Results: Our results provide experimental evidence that GM-CSF inhibits growth and migration, as well as induction of apoptosis in EC cells. In addition, EC cells stimulated with GM-CSF were more likely to have suppressed epithelial-to-mesenchymal transition (EMT), accompanied by increased E-cadherin and decreased vimentin expression. Conclusion: Our data demonstrate that GM-CSF inhibits cancer cell proliferation and migration, as well as induction of apoptosis. Moreover, our findings indicate that GM-CSF may regulate EMT through JAK2-PRMT5 signaling, and thereby exhibit its antitumor effects on EC cells.
机译:目的:最新研究证明粒细胞巨噬细胞集落刺激因子(GM-CSF)可能具有抗肿瘤作用;但是,确切的机制仍不清楚。我们的研究目的是分析GM-CSF对人食道癌(EC)细胞系多种生物学功能的影响,并探讨其抗肿瘤作用的潜在机制。材料和方法:检查Eca109 / 9706人EC细胞。分别使用细胞增殖测定,流式细胞术和transwell测定来分析细胞增殖,凋亡和迁移。通过逆转录聚合酶链反应和蛋白质印迹检查信号分子的表达。结果:我们的结果提供了实验证据,表明GM-CSF抑制EC细胞的生长和迁移以及诱导细胞凋亡。此外,用GM-CSF刺激的EC细胞更有可能抑制了上皮到间质转化(EMT),并伴有E-钙粘蛋白增加和波形蛋白表达降低。结论:我们的数据表明GM-CSF抑制癌细胞的增殖和迁移以及诱导细胞凋亡。此外,我们的发现表明,GM-CSF可能通过JAK2-PRMT5信号传导调节EMT,从而表现出其对EC细胞的抗肿瘤作用。

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