PEBP4 enhanced HCC827 cell proliferation and invasion ability and inhibited apoptosis

PEBP4 enhanced HCC827 cell proliferation and invasion ability and inhibited apoptosis
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DOI:
10.1007/s13277-012-0514-0
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发表时间:
2013-02
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影响因子:
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通讯作者:
Guiping Yu;Zhenya Shen;Guo-qiang Chen;Xiaomei Teng;Yanqiu Hu;Bin Huang
Guiping Yu;Zhenya Shen;Guo-qiang Chen;Xiaomei Teng;Yanqiu Hu;Bin Huang
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文献类型:
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作者:
Guiping Yu;Zhenya Shen;Guo-qiang Chen;Xiaomei Teng;Yanqiu Hu;Bin Huang

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本研究的目的是探讨磷脂酰乙醇胺结合蛋白4(PEBP4)对非小细胞肺癌(NSCLC)细胞生长、增殖、凋亡和侵袭的影响,为未来NSCLC的治疗选择提供依据。进行蛋白质印迹测定以检查 NSCLC 细胞系(HCC827、A549、NCI-H661、NCI-H292 和 95-D)和正常人支气管上皮 (HBE) 细胞系中的 PEBP4 蛋白表达水平。构建PEBP4 shRNA表达载体并转染HCC827细胞。随后,使用 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物测定、流式细胞术分析和 Transwell 侵袭测定分析 PEBP4 对 HCC827 细胞的细胞活力、细胞周期分布、凋亡水平和侵袭特性的影响。此外,还研究了PEBP4对细胞周期蛋白D1、p53、Bcl-2、MMP-2和MMP-9等蛋白表达的影响。 PEBP4在肺癌细胞(HCC827、A549、NCI-H661、NCI-H292和95-D)中高表达,但在HBE细胞中低表达。 PEBP4敲低组HCC827细胞的细胞活力、细胞增殖和侵袭能力均显着低于阴性对照组和空白对照组(p< 0.05),且阴性对照组和空白对照组细胞活力、细胞增殖、凋亡和侵袭能力无显着差异。在HCC827细胞中,PEBP4敲低组cyclin D1、Bcl-2、MMP-2、MMP-9表达量显着降低(p< 0.05),p53蛋白表达量显着高于阴性对照组和空白对照组(p< 0.05)。阴性对照组和空白对照组间cyclin D1、p53、Bcl-2、MMP-2、MMP-9的表达水平无显着差异。总之,PEBP4增强HCC827细胞增殖和侵袭能力并抑制细胞凋亡。 PEBP4表达降低可能与人NSCLC细胞系HCC827侵袭能力降低和凋亡增加有关。
The purposes of this study were to investigate the effects of phosphatidylethanolamine-binding protein 4 (PEBP4) on the cell growth, proliferation, apoptosis, and invasion of non-small cell lung cancer (NSCLC) cells and to provide evidence for future treatment options for NSCLC. Western blot assays were performed to examine PEBP4 protein expression levels in NSCLC cell lines (HCC827, A549, NCI-H661, NCI-H292, and 95-D) and a normal human bronchial epithelial (HBE) cell line. A PEBP4 shRNA expression vector was constructed and transfected into HCC827 cells. Subsequently, the effects of PEBP4 on the cell viability, cell cycle distribution, apoptosis levels, and invasion properties of HCC827 cells were analyzed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays, flow cytometry analyses, and transwell invasion assays. In addition, the effects of PEBP4 on the expression of proteins including cyclin D1, p53, Bcl-2, MMP-2, and MMP-9 were investigated. PEBP4 was highly expressed in lung cancer cells (HCC827, A549, NCI-H661, NCI-H292, and 95-D), but its expression was low in HBE cells. Cell viability, cell proliferation, and invasion of HCC827 cells in the PEBP4 knockdown group were significantly lower than that in the negative control and blank control groups (p< 0.05), and there were no significant differences between the negative and blank control groups in terms of cell viability, cell proliferation, apoptosis, and invasion. In HCC827 cells, the expression levels of cyclin D1, Bcl-2, MMP-2, and MMP-9 in the PEBP4 knockdown group were significantly lower (p< 0.05), and the expression of p53 protein was significantly higher than that in the negative and blank control groups (p< 0.05). There were no significant differences between the negative and blank control groups in the expression levels of cyclin D1, p53, Bcl-2, MMP-2, and MMP-9. In conclusion, PEBP4 enhanced HCC827 cell proliferation and invasion ability and inhibited apoptosis. Decreased PEBP4 expression may play a role in the reduced invasion ability and increased apoptosis of the human NSCLC cell line HCC827.