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低氧对人肺腺癌A549多细胞球体上皮-间质转化促转移的影响 被引量:4

The influence of hypoxia on metastasis induced by epithelial-mesenchymal transition of human lung adenocarcinoma A549 cell spheres
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摘要 目的:探讨低氧对人肺腺癌A549细胞来源的A549多细胞球体上皮-间质转化(epithelial-mesenchymal transition,EMT)促转移机制的影响。方法:采用无血清培养(serum-freemedium,SFM)的方法培养A549细胞,诱导A549多细胞球体形成;随后将亲本A549细胞和A549多细胞球体在低氧环境下培养24h,分别检测2种细胞中EMT标志物E-钙黏着素(E-cadherin)和波形蛋白(vimentin)的表达水平,并与它们在常氧条件下的表达情况进行比较。结果:在常氧和低氧条件下,A549多细胞球体中E-cadherinmRNA和蛋白的表达水平均较亲本A549细胞降低,而vimentin的表达水平升高;与常氧条件相比,低氧培养的亲本A549细胞及A549多细胞球体中E-cadherinmRNA和蛋白的表达水平均下调,且以A549多细胞球体下调更为明显,而vimentin的表达水平则升高。结论:A549多细胞球体比亲本A549细胞具有更强的转移能力,低氧条件下A549多细胞球体比常氧条件下的A549多细胞球体具有更强的转移能力。 Objective: To investigate the influence of hypoxia on metastasis induced by epithelialmesenchymal transition of human lung adenocarcinoma A549 cell spheres. Methods: A549 cell spheres were formed through serum-free culture. The expression levels of E-cadherin and vimentin in the parental A549 cells and A549 sphere cells under hypoxia condition for 24 h were examined by immunofluorescence, Western blotting, and reverse transcription (RT)-PCR, and compared with the expressions levels under normoxia condition. Results: Under hypoxia and normoxia conditions, the expression levels of E-cadherin mRNA and protein in the A549 cells spheres were lower than those in the parental A549 cells, but the expression levels of vimentin mRNA and protein in the A549 cell spheres were increased. As compared with the normoxic condition, the expression levels of E-cadherin mRNA and protein in the parental A549 cells and the A549 cell spheres were all down-regulated under hypoxic condition, and especially for the parental A549 cells, this decline was much more obvious; while the expression level of vimentin was increased. Conclusion: A549 cell spheres have a stronger ability of metastasis than the parental A549 cells. This ability of metastasis is also stronger in the A549 cell spheres under hypoxic condition than that in the parental A549 cells under normoxia.
出处 《肿瘤》 CAS CSCD 北大核心 2012年第3期182-188,共7页 Tumor
基金 江西省教育厅科学技术研究基金资助项目(编号:GJJ10345)
关键词 肺肿瘤 细胞上皮-间质转化 干细胞 细胞低氧 A549细胞 Lung neoplasms Epithelial-mesenchymal transition Stem cells Cell hypoxia A549 cells
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  • 1张惠忠,华平,李海刚,吕志强,曾韵洁,刘金耿,曾弘.非小细胞肺癌血管内皮生长因子-C和环氧合酶-2蛋白的表达及其对预后的影响[J].中华肿瘤杂志,2005,27(12):734-737. 被引量:14
  • 2丁建春,陈宇宁,孙梅.环氧化酶2与缺氧诱导因子1α在肺腺癌中的表达与相关性[J].江苏医药,2007,33(2):129-131. 被引量:2
  • 3CLARKE M F, DICK J E, DIRKS P B, et al. Cancer stem cells-perspectives on current status and future directions: AACR workshop on cancer stem celrs[J]. Cancer Res, 2006, 66 (19): 9339-9344.
  • 4AI-HAJJ M, WlCHA M S, BENITO-HERNANDEZ A, et al. Prospective identification of tumorigenic b'reast cancer cells[J]. Proc Natl Acad Sci USA, 2003, 100(7): 3983-3988.
  • 5DEAN M, FOJO T, BATES S. Tumour stem cells and drug resistance[J]. Nat Rev Cancer, 2005, 5(4): 275-284.
  • 6ERAMO A, LOTTI F, SETTE G, et al. Identification and expansion of the tumorigenic lung cancerstem cell population[J]. Cell Death Differ, 2008, 15(3): 504-514.
  • 7YU S C, PING Y F, YI L, et al. Isolation and characterization of cancer stem cells from a human glioblastoma cell line U87[J]. Cancer Lett, 2008, 265(1):124-134.
  • 8YANG L, ZHOU X, YANG J, et al. Aspirin inhibits cytotoxicity of prion peptide PrP106-126 to neuronal cells associated with microglia activation in vitro[J]. J Neuroimmunol, 2008, 199(1/2): 10-17.
  • 9ZHAO C, CHEN A, JAMIESON C H, eta/. Hedgehog signalling is essential for maintenance of cancer stem cells in myeloid leukaemia[J]. Nature, 2009, 458(7239): 776-779.
  • 10GAVIRAGHI M, TUNICI P, VALENSIN S, et al. Pancreatic cancer spheres are more than just aggregates of stem marker positive cells[J]. BiosciRep, 2010, 31(1): 45-55.

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  • 1郑必强,周瑾,耿沁,董强刚.人肺腺癌干细胞源自肺脏细支气管肺泡干细胞的初步研究[J].中国肺癌杂志,2008,11(6):759-764. 被引量:12
  • 2赵欣.载microRNA-34a脂质体靶向治疗肺癌干细胞靶的研究[J].中国生化药物杂志,2014,34(1):68-71. 被引量:11
  • 3蔡华荣,江跃全.多肽修饰载紫杉醇脂质体靶向A549肺癌干细胞的研究[J].中国生化药物杂志,2014,34(4):11-14. 被引量:5
  • 4Feng Li,Benjamin Tiede,Joan Massague,Yibin Kang.Beyond tumorigenesis: cancer stem cells in metastasis[J].Cell Research,2007,17(1):3-14. 被引量:86
  • 5FORONI C, BROGGINI M, GENERALI D, et al. Epithelial- mesenchymal transition and breast cancer: role, molecular mechanisms and clinical impact[J]. Cancer Treat Rev, 2012, 38(6):689-697.
  • 6VINCENT-SALOMON A, THIERY J P. Host microenvironment in breast cancer development: epithelial-mesenchymal transition in breast cancer development[J]. Breast Cancer Res, 2003, 5(2):101-106.
  • 7VALCOURT U, KOWANETZ M, NIIMI H, et al. TGF-beta and the Smad signaling pathway support transcriptomic reprogramming during epithelial-mesenchymal cell transition[J]. Mol Biol Cell, 2005, 16(4):1987-2002.
  • 8NAWSHAD A, LAGAMBA D, POLAD A, et al. Transforming growth factor-β signaling during epithelial-mesenchymal transformation: implications for embryogenesis and tumor metastasis[J]. Cells Tissues Organs, 2005,1 79(1-2):11-23.
  • 9DIMEO T A, ANDERSON K, PHADKE P, et al. A novel lung metastasis signature links Wnt signaling with cancer cell self-renewal and epithelial-mesenchymal transition in basal-like breast cancer[J]. Cancer Res, 2009, 69(13):5364-5373.
  • 10HUBER M A, BEUG H, WlRTH T. Epithelial-mesenchymal transition: NF-kappaB takes center stageD]. Cell Cycle, 2004, 3(12):1477-1480.

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