| 吴守振 李海龙 张阔 张旺倩 薛晓畅 张伟 张英起.EPO/EPOR 在非小性细胞肺癌发展中的作用研究[J].现代生物医学进展英文版,2015,15(28):5428-5431. |
| EPO/EPOR 在非小性细胞肺癌发展中的作用研究 |
| The Effect of EPO/EPOR on the Progressionof Nonsmall Cell Lung Cancer (NSCLC) |
| |
| DOI： |
| 中文关键词: EPO EPOR NSCLC 细胞周期 |
| 英文关键词: EPO EPOR NSCLC Cell cycle |
| 基金项目:国家自然科学基金项目（81100001） |
|
| Hits: 830 |
| Download times: 0 |
| 中文摘要: |
| 目的：研究促红细胞生成素（erythropoietin, EPO）及其受体（EPOR）在非小性细胞肺癌中的生物学作用。方法：收集27 例非小
性细胞肺癌（NSCLC），免疫组织化学方法检测肺癌组织中EPO 和EPOR的表达；观察人源重组EPO（rhEPO）对HCC15 和
HCC1819 细胞活力和细胞周期的影响；分析缺氧对NSCLC细胞EPO 及EPOR 表达的影响。结果：27例非小细胞肺癌的组织标
本中13 例表达EPO，表达率为48 %，25 例表达EPOR，表达率为92 %。rhEPO明显增加了高表达EPOR 的HCC1819 细胞克隆
数，而对低表达EPOR 的HCC15 细胞的克隆形成没有影响。rhEPO增强了HCC1819 的细胞活力，但以siRNA干涉HCC1819
EPOR后，EPO对HCC1819 细胞活力增强作用消失。rhEPO 明显增加了HCC1819 细胞的细胞周期。缺氧促进了HCC1819 细胞的
EPO 的表达，增强了细胞活力。结论：EPO 和EPOR在非小性细胞肺癌中表达增高，EPO 通过EPOR 促进了NSCLC 细胞的增殖，
缺氧诱导了NSCLC 细胞EPO的表达。 |
| 英文摘要: |
| Objective:To investigate the bio-function of EPO and EPOR in the cancer progression of NSCLC.Methods:NSCLC tissues were recruited. The expression levels of EPO and EPOR were analyzed in 27 NSCLC tissues by immunohistochemistry
(IHC). The cell viability and cell cycle were detected in HCC15 and HCC1819 cells under recombinant human EPO (rhEPO). EPO and
EPOR expression were observed in HCC15 and HCC1819 under hypoxia.Results:EPO and EPO-R expression were up-regulated in
NSCLC samples. The expression rate of EPO expression was observed in 48% (13 of 27) NSCLC. The expression rate of EPOR was
up-regulated in 92% (25 of 27) NSCLC. In vitro, rhEPO obviously increased the numbers of colony formation of EPOR up-regulating
HCC1819 cells, whereas rhEPO had no effect on the numbers of colony formation of EPOR down-regulating HCC15 cells. Meanwhile,
rhEPO enhanced the viability of HCC1819 cells. Knockdown of EPOR via siRNA decreased the viability induced by rhEPO. rhEPO
significantly promoted HCC1819 cell cycle. Hypoxia up-regulated EPO expression and then increased cell viability in HCC1819 cells.Conclusion:EPO and EPOR are up-regulated in NSCLC. EPO promotes cancer progression of NSCLC via EPOR. Hypoxia increases the
levels of EPO in NSCLC. |
|
View Full Text
View/Add Comment Download reader |
| Close |
