首页> 外文期刊>International journal of molecular medicine >Radiosensitizing effects of Cyclocarya paliurus polysaccharide on hypoxic A549 and H520 human non-small cell lung carcinoma cells
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Radiosensitizing effects of Cyclocarya paliurus polysaccharide on hypoxic A549 and H520 human non-small cell lung carcinoma cells

机译:环核糖菌多糖对缺氧A549和H520人非小细胞肺癌细胞的辐射敏感效应

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摘要

Cyclocarya paliurus (CP) polysaccharide (CPP) is a chemical component contained in CP, which has been reported to possess significant hypoglycemic activity. The present study aimed to investigate the radiosensitizing effect and underlying mechanisms of CPP on hypoxic A549 and H520 human non-small cell lung carcinoma cells. Cell viability, apoptosis and proliferation were determined using Cell Counting kit-8 assay, flow cytometry and colony formation assay, respectively. mRNA and protein expression levels were determined by reverse transcription-quantitative PCR and western blot analysis, respectively. The results suggested that CPP markedly inhibited the viability of hypoxic A549 and H520 cells. In response to combined treatment with CPP and radiation, hypoxic A549 and H520 cells exhibited enhanced apoptosis; in addition, cell proliferation was suppressed and the expression levels of hypoxia-inducible factor-1 alpha, survivin and cleaved caspase-3 were modified. Furthermore, CPP in combination with radiation affected the mammalian target of rapamycin (mTOR)/Akt/phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) pathway. These findings indicated that CPP may enhance the radiosensitivity of hypoxic A549 and H520 cells; this effect may be associated with inhibition of the mTOR/Akt/PI3K pathway. The potential radiosensitizing effects of CPP on hypoxic A549 and H520 cells suggested that CPP may be an effective target for treatment of non-small cell lung carcinoma.
机译:环核菌(CP)多糖(CPP)是CP中含有的化学成分,据报道据报道具有显着的降血糖活性。本研究旨在探讨CPP对缺氧A549和H520人非小细胞肺癌细胞的辐射敏化效应和潜在机制。使用细胞计数试剂盒-8测定法测定细胞活力,细胞凋亡和增殖,流式细胞术和菌落形成测定法测定。通过逆转录定量PCR和Western印迹分析分别测定mRNA和蛋白表达水平。结果表明,CPP显着抑制缺氧A549和H520细胞的活力。响应于CPP和辐射的组合治疗,缺氧A549和H520细胞表现出增强的细胞凋亡;此外,抑制了细胞增殖,并改变了缺氧诱导因子-1α,Survivin和切割的Caspase-3的表达水平。此外,CPP与辐射相结合影响了雷帕霉素(MTOR)/ AKT /磷脂酰肌醇-4,5-双磷酸三磷酸溶胶(PI3K)途径的哺乳动物靶标。这些发现表明CPP可以增强缺氧A549和H520细胞的放射敏感性;该效果可能与MTOR / AKT / PI3K途径的抑制相关。 CPP对缺氧A549和H520细胞的潜在放射敏化作用表明CPP可以是治疗非小细胞肺癌的有效靶标。

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