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作 者:李晓敏[1] 于哲[2] 何金萍[1] 曹珊珊 槐梅 马艳奇 LI Xiaomin;YU Zhe;HE Jinping(Department of Pathology,North China Petroleum Administration Bureau General Hospital,Hebei,Renqiu 062552,China;不详)
机构地区:[1]华北石油管理局总医院病理科,河北省任丘市062552 [2]华北石油管理局总医院普胸科,河北省任丘市062552 [3]华北石油管理局总医院体检中心,河北省任丘市062552
出 处:《河北医药》2023年第17期2612-2615,共4页Hebei Medical Journal
基 金:河北省卫生健康委员会项目(编号:20190114)。
摘 要:目的肿瘤细胞缺氧微环境与肺癌的发展和转移密切相关,探讨肺癌中NUSAP1在细胞缺氧调控中的作用。方法利用CoCl_(2)处理肺癌A549细胞模拟肿瘤细胞缺氧,并利用小RNA干扰技术敲低缺氧细胞中NUSAP1的表达,分别采用CCK8、transwell、流式细胞术检测细胞增殖、迁移和侵袭及细胞凋亡的变化。结果经CoCl_(2)处理后,A549细胞的增殖、迁移和侵袭能力显著增加,而凋亡能力显著下降。在缺氧细胞中敲低NUSAP1后,与缺氧组比较,细胞的增殖、迁移和侵袭能力显著下降,而细胞凋亡数量显著上升,差异有统计学意义(P<0.05)。结论敲低NUSAP1可以抑制由缺氧引起的细胞增殖和转移,提示NUSAP1是肿瘤缺氧调控的下游潜在靶点之一。Objective The hypoxic microenvironment of tumor cells is closely related to the development and metastasis of lung cancer.This study aims to explore the role of nucleolar and spindle associated protein 1(NUSAP1)in regulating cellular hypoxia in lung cancer.Methods Lung cancer a549 cells were treated with cobalt chloride(CoCl2)to simulate hypoxia.The small interfering RNA technology was used to knock down the expression of NUSAP1 in hypoxic cells.The cell proliferation,migration and invasion,and apoptosis were detected by Cell Counting Kit-8(CCK-8)assay,Transwell assay and flow cytometry,respectively.Results After treatment with CoCl_(2),the proliferation,migration and invasion of A549 cells were significantly promoted,while the apoptosis ability was significantly reduced.After knockdown of NUSAP1 in hypoxic cells,the proliferation,migration and invasion ability of the cells were significantly reduced compared with the hypoxic group,and the number of apoptosis was significantly enhanced(P<0.05).Conclusion Knockdown of NUSAP1 can inhibit proliferation and metastasis in lung cancer cells caused by hypoxia,suggesting that NUSAP1 is one of the downstream potential targets for tumor hypoxia regulation.
关 键 词:细胞缺氧 肺癌 核仁纺锤体相关蛋白1 NUSAP1 细胞凋亡
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