Department of Medical Imaging, Liaocheng People's Hospital, Liaocheng, Shandong 252002, P.R. China.
Int J Mol Med. 2019 Oct;44(4):1233-1242. doi: 10.3892/ijmm.2019.4289. Epub 2019 Jul 26.
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‑1α, 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.
青钱柳多糖(CPP)是青钱柳中含有的一种化学成分,据报道具有显著的降血糖活性。本研究旨在探讨 CPP 对缺氧 A549 和 H520 人非小细胞肺癌细胞的放射增敏作用及其机制。分别采用细胞计数试剂盒-8 检测法、流式细胞术和集落形成实验检测细胞活力、凋亡和增殖。采用逆转录-定量 PCR 和 Western blot 分析分别检测 mRNA 和蛋白表达水平。结果表明,CPP 显著抑制缺氧 A549 和 H520 细胞的活力。与 CPP 和辐射联合治疗后,缺氧 A549 和 H520 细胞凋亡增强;此外,细胞增殖受到抑制,缺氧诱导因子-1α、存活素和裂解 caspase-3 的表达水平发生改变。此外,CPP 联合辐射影响哺乳动物雷帕霉素靶蛋白(mTOR)/Akt/磷脂酰肌醇-4,5-二磷酸 3-激酶(PI3K)通路。这些发现表明,CPP 可能增强缺氧 A549 和 H520 细胞的放射敏感性;这种作用可能与抑制 mTOR/Akt/PI3K 通路有关。CPP 对缺氧 A549 和 H520 细胞的潜在放射增敏作用表明,CPP 可能是治疗非小细胞肺癌的有效靶点。