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SRPK1 Dissimilarly Impacts on the Growth Metastasis Chemosensitivity and Angiogenesis of Glioma in Normoxic and Hypoxic Conditions

机译:SRPK1对常氧和低氧条件下胶质瘤的生长转移化学敏感性和血管生成有不同的影响

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摘要

Glioma is among the ten most common causes of cancer-related death and has no effective treatment for it, so we are trying to find a new target for anticancer treatment. This study investigates the different expression of SRPK1 as a novel protein in glioma, which can influence tumor cells biological characteristics in normoxic and hypoxic environment. The expression levels of SRPK1 protein in glioma cell lines transfected with siSRPK1 or not were examined using immunofluorescence, RT-PCR and Western blot analysis, respectively. The impact of SRPK1 on the biological characteristics of U251 cells was further studied using methylthiazol tetrazolium assays, flow cytometry, and Transwell invasion chamber assays. The results showed that knockdown of SRPK1 inhibited tumor cells growth, invasion and migration in normoxic condition, but portion of the effect could be reversed in hypoxia. SRPK1 expression was induced in glioma cells by DDP treated, but not TMZ, in both normoxia and hypoxia conditions. We propose SRPK1 as a new molecular player contributing to the early treatment of glioma.
机译:胶质瘤是癌症相关死亡的十种最常见原因之一,目前尚无有效的治疗方法,因此我们正在尝试寻找新的抗癌治疗靶标。这项研究调查了神经胶质瘤中SRPK1作为一种新型蛋白的不同表达,这可能影响正常氧和低氧环境中肿瘤细胞的生物学特性。分别使用免疫荧光,RT-PCR和Western印迹分析检测了是否用siSRPK1转染的神经胶质瘤细胞系中SRPK1蛋白的表达水平。使用甲基噻唑四唑鎓测定,流式细胞术和Transwell侵入室测定进一步研究了SRPK1对U251细胞生物学特性的影响。结果表明,敲低SRPK1可以在常氧条件下抑制肿瘤细胞的生长,侵袭和迁移,但在缺氧条件下,部分效应可以逆转。在常氧和低氧条件下,DDP处理可诱导胶质瘤细胞SRPK1表达,而TMZ则不。我们建议SRPK1作为促进神经胶质瘤早期治疗的新分子。

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