首页> 外文期刊>Lung cancer: Journal of the International Association for the Study of Lung Cancer >Imatinib inhibits in vitro proliferation of cells derived from a pleural solitary fibrous tumor expressing platelet-derived growth factor receptor-beta.
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Imatinib inhibits in vitro proliferation of cells derived from a pleural solitary fibrous tumor expressing platelet-derived growth factor receptor-beta.

机译:伊马替尼抑制表达表达血小板源性生长因子受体-β的胸膜孤立性纤维瘤的细胞的体外增殖。

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摘要

We examined the in vitro effects of imatinib (Novartis Pharma AG, Basel, Switzerland) as a possible inhibitor of PDGFR pathway on cells derived from a recurrence of a pleural malignant solitary fibrous tumor (SFT). Primary cell culture was characterised by immunofluorescence. SFT-derived cells were treated with imatinib at different time points. Western blotting for PDGFR-beta, phospho-PDGFR-beta or smooth muscle actin (SMA) was performed before and after 96 h of treatment with imatinib. SFT-derived cells treated with imatinib for 96 h showed a dose dependent decrease of Ki67 expression. Results were confirmed by growth curve. Western blotting showed that PDGFR-beta was highly expressed and phosphorylated in SFT-derived cells and imatinib treatment reduced PDGFR-beta phosphorylation and SMA expression. With the limit of experimental findings, our results support a possible future application of imatinib as a candidate molecule in the target therapy of malignant SFTs over-expressing wild-type PDGFR.
机译:我们检查了伊马替尼(Novartis Pharma AG,巴塞尔,瑞士)作为PDGFR途径的可能抑制剂对源自胸膜恶性孤立性纤维性肿瘤(SFT)复发的细胞的体外作用。原代细胞培养的特征在于免疫荧光。在不同的时间用伊马替尼处理SFT衍生的细胞。用伊马替尼治疗96小时之前和之后,对PDGFR-β,磷酸-PDGFR-β或平滑肌肌动蛋白(SMA)进行蛋白质印迹。用伊马替尼处理96 h的SFT衍生细胞显示Ki67表达呈剂量依赖性降低。生长曲线证实了结果。蛋白质印迹显示PDGFR-β在SFT衍生的细胞中高度表达和磷酸化,伊马替尼治疗降低了PDGFR-β的磷酸化和SMA表达。由于实验结果的局限性,我们的研究结果支持伊马替尼作为候选分子在过度表达野生型PDGFR的恶性SFT靶标治疗中的可能应用。

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