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缺氧对人乳腺癌细胞微球体成瘤性的影响及机制研究

Study of the impacts and mechanism of hypoxia on tumorigenicity of human breast cancer cells mammospheres
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摘要 目的研究缺氧状态对人乳腺癌细胞微球体(MSs)成瘤性的影响,进一步探讨产生这种影响的可能机制。方法在缺氧及常氧状态下对接受过化疗的人乳腺癌细胞进行无血清悬浮培养,将获得的微球体细胞(MSDCs)注入小鼠背部两侧以观察其成瘤情况,RT-PCR及Western blot检测移植瘤细胞增殖相关基因及蛋白表达水平。结果缺氧组MSDCs的成瘤性强于常氧组,Western blot及RT-PCR检测结果提示,缺氧组MSDCs中低氧诱导因子-2α(HIF-2α)、三磷酸腺苷结合转运蛋白G超家族成员2抗体(ABCG2)、表皮细胞生长因子(EGF)、血管内皮生长因子(VEGF)蛋白及mRNA的表达水平高于常氧组(P<0.05)。结论缺氧可能通过影响MSDCs中HIF-2α、ABCG2、EGF、VEGF表达水平,从而增强MSDCs的成瘤性。 Objective To study the effect of hypoxia on the tumorigenesis of human breast cancer mammospheres(MSs),and to further explore the possible mechanism of this effect.Methods Under hypoxia and normoxia status,chemotherapy human breast cancer tissue cells were cultured in suspension in a serum-free medium,and the obtained microspheres-derived cells(MSDCs)were injected into both sides of the back of mice to observe their tumor formation.The expression levels of HIF-2α,ABCG2,EGF,VEGF in the transplanted tumors were tested by Western blot and RT-PCR.Results The tumorigenicity of MSDCs in the hypoxia group was stronger than those in the normoxia group.The protein and mRNA expression levels of HIF-2α,ABCG2,EGF,VEGF in the normoxia group were higher than that of the hypoxia group normoxia(P<0.05).Conclusion Hypoxia is likely to enhance the tumorigenicity of MSDCs by affecting the expression of HIF-2α,ABCG2,EGF,VEGF.
作者 谢佳良 范原铭 吴兰 侯婧 徐宏宇 罗小红 XIE Jialiang;FAN Yuanming;WU Lan;HOU Jing;XU Hongyu;LUO Xiaohong(The Second Department of General Surgery,People′s Hospital of Changshou District,Chongqing 401220,China;Department of Oncology,People′s Hospital of Changshou District,Chongqing 401220,China;Department of Pathology,People′s Hospital of Changshou District,Chongqing 401220,China)
出处 《重庆医学》 CAS 2020年第18期2997-3001,共5页 Chongqing medicine
基金 重庆市卫生和计划生育委员会医学科研项目(2017ZBXM025)。
关键词 乳腺肿瘤 肿瘤干细胞 低氧 缺氧诱导因子2α 三磷酸腺苷结合转运蛋白G超家族成员2 表皮生长因子 血管内皮生长因子A breast tumor neoplastic stem cells hypoxia hypoxia inducible factor-2α ABCG2 epidermal growth factor vascular endothelial growth eactor A
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