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顺铂对结直肠癌细胞增殖及侵袭能力的影响 被引量:2

Effects of Cisplatin on Proliferation and Invasion of Colorectal Cancer Cells
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摘要 目的探讨顺铂对人结直肠癌细胞SW480增殖及侵袭力的影响。方法以SW480细胞为研究对象,设定未经处理的SW480细胞为对照组,给予不同浓度顺铂进行不同时间干预,应用MTT法、Transwell侵袭小室、定磷法检测SW480细胞的增殖、侵袭力及Na+-K+-ATP酶活性。结果生理浓度顺铂(70μmol/L)在48 h即可抑制SW480细胞的增殖,与72和96 h相比抑制率差异无统计学意义;70μmol/L顺铂处理48 h时,即可降低穿越Matrigel膜基质的细胞数;分别采用17.5、35、70和140μmol/L4个梯度浓度的顺铂作用于SW480细胞48 h后,35、70和140μmol/L组细胞中Na+-K+-ATP酶活性均显著升高,且顺铂浓度达70μmol/L时Na+-K+-ATP酶即可达到较高活性。结论 Na+-K+-ATP酶活性的降低可能导致对结直肠癌细胞增殖和侵袭能力调节作用减弱,可能与结直肠癌细胞SW480耐顺铂有关。 Objective To investigate the effect of cisplatin on proliferation and invasion of colorectal cancer cell line SW480. Methods SW480 cells were used as the research object, and untreated SW480 cells were used as the control group. Different concentrations of cisplatin was given at different times to intervene. The MTT, Transwell chamber and phos-phate determination methods were used to detect proliferation, invasion and Na+-K+-ATPase activity expression level in SW480 cells. Results The physiological concentration of cisplatin (70 μmol/L) inhibited the proliferation of SW480 cells at 48 h. There was no significant difference in the inhibition rate at 48 h compared with 72 h and 96 h. Treatment with 70 μmol/L cisplatin for 48 h reduced the number of cells through Matrigel membrane matrix. The Na+-K+-ATPase activity was significantly increased in 35, 70 and 140 μmol/L cells after treatment with 17.5, 35, 70 and 140 μmol/L of cisplatin in SW480 cells for 48 h, and Na+-K+-ATPase reached the highest level at 70 μmol/L of cisplatin. Conclusion The decreased activity of Na+-K+-ATPase may lead to the attenuation in proliferation and invasion of colorectal cancer cells, which may be associated with cisplatin resistance in colorectal cancer cell SW480.
作者 徐阳
出处 《天津医药》 CAS 北大核心 2014年第7期638-640,共3页 Tianjin Medical Journal
关键词 结直肠肿瘤 顺铂 细胞增殖 肿瘤侵润 抗药性 肿瘤 SW480 NA+-K+-ATP酶 SW480 colorectal neoplasms cisplatin cell proliferation neoplasm invasiveness drug resistance,neoplasm Na+-K+-ATPase
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  • 1Edwards BK, Ward E, Kohler BA, et al. Annual report to the nation on the status of cancer, 1975-2006, featuring colorectal cancer trends and impact of interventions (risk factors, screening, and treat- ment) to reduce future rates[J]. Cancer, 2010, 116(3): 544-573. doi: 10.10021cncr.24760.
  • 2Tveit KM, Guren T, Glimelins B, et al. Phase III trial of cetuximab with continuous or intermittent fluorouraeil, leucovorin, and oxalipl- atin (Nordic FLOX) versus FLOX alone in first-line treatment of metastatic colorectal cancer: the NORDIC-VII study[J]. J Clin On-col, 2012, 30(15): 1755-1762.doi: 10.1200/JC0.2011.38.0915.
  • 3American Cancer Society.Cancer Facts and Fig.s 2012 U. S.[J/OL] http://www.cancer.org/research/cancerfactsfigures/cancerfactsfigur es/cancer-facts-figures-2012.
  • 4Nannizzi S, Veal GJ, Giovannetti E, et al. Cellular and molecular mechanisms for the synergistic cytotoxicity elicited by oxaliplatin and pemetrexed in colon cancer cell lines[J]. Cancer Chemother Pharma- col, 2010, 66(3): 547-558.doi: 10.1007/s00280-009-1195-2.
  • 5张贵海,张先平,文坤明,胡敏,王轶,藏春宝,李少林.哇巴因抑制结直肠癌多药耐药细胞增殖及侵袭力的研究[J].中国肿瘤临床,2012,29(5):254-258. 被引量:2
  • 6唐春兰,杨和平,周向东.DNA损伤修复与肺癌顺铂耐药机制的研究进展[J].中国肺癌杂志,2011,14(12):960-964. 被引量:34
  • 7Calder6n GD, Esquivel GJ, Garcia EH, et al. Effects of marijuana and diazepam on lipid peroxidation, Na+, K+ ATPase, and levels of glutathione and 5-HTP in rat brain[J]. Acta BiolHung, 2010, 61(2): 135-144.doi: 10.1556/ABiol.61.2010.2.2.
  • 8Hayward-Lester AL. Analysis of sodium pump gene expression in microdissected nephrons using competitive RT-PCR and a novel I-IPLC technique[M]. USA:UMI,1997.
  • 9Ahmed Z, Deyama Y, Yoshimura Y, et al. Cisplatin sensitivity of oral squamous carcinoma ceils is regulated by Na+, K+-ATPase ac- tivity rather than copper-transporting P-type ATPases, ATPTA and ATP7B[J]. Cancer Chemother Pharmacol, 2009, 63(4): 643-650. doi: 10.1007/s00280-008-0781-z.
  • 10Morth JP, Pedersen BP, Buch-Pedersen MJ, et al. A structural over- view of the plasma membrane Na+-K+-ATPase and H+-ATPase ion pumps[J]. Nat Rev Mol Cell Biol, 2011, 12(1): 60-70.doi: 10.1038/ nrm3031.

二级参考文献16

  • 1Geering K.The functional role of beta subunits in oligomeric P-type ATPase[J].J Bioenerg Biomembr,2001,33(5):425-438.
  • 2Kitamura N,Ikekita M,Sato T,et al.Mouse Na +/K +-ATPase β 1-subunit has a K +-dependent cell adhesion activity for β-GlcNActerminating glycans[J].Proc Natl Acad Sci U S A,2005,102(8):2796-2801.
  • 3Shoshani L,Contreras RG,Roldan ML,et al.The polarized expression of Na+,K+-ATPase in epithelia depends on the association between β-subunits located in neighboring cells[J].Mol Biol Cell,2005,16(3):1071-1081.
  • 4Rajasekaran SA,Huynh TP,Wolle DG,et al.Na,K-ATPase Subunits as Markers for Epithelial-Mesenchymal Transition in Cancer and Fibrosis[J].Mol Cancer Ther,2010,9(6):1515-1524.
  • 5Inge LJ,Rajasekaran SA,Yoshimoto K,et al.Evidence for a potential tumor suppressor role for the Na,K-ATPase β1-subunit[J].Histol Histopathol,2008,23(4):459-467.
  • 6Espineda C,Seligson DB,Ball Jr.JW,et al.Analysis of the Na,K-ATPase α-and β-subunit expression profiles of bladder cancer using tissue microarrays[J],Cancer,2003,97(8):1859-1868.
  • 7Espineda C,Chang JH,Twis J,et al.Repression of Na,K-ATPase β1-subunit by the transcription factor Snail in carcinoma[J].Mo Biol Cell,2004,15(2):1364-1373.
  • 8Aperia A.New roles for an old enzyme:Na,K-ATPase emerges as an interesting drug target[J].J Intern Med,2007,261(1):44-52.
  • 9Liu J,Tian J,Haas M,et al.Ouabain interaction with cardiac Na+/K+-ATPase initiates signal cascades independent of changes in intracellular Na+ and Ca2 + concentrations[J].J Biol Chem,2000,275(36):27838-27844.
  • 10Yang AD,Fan F,Camp ER,et al.Chronic Oxaliplatin Resistance Induces Epithelial-to-Mesenchymal Transition in Colorectal Cancer Cell Lines[J].Clin Cancer Res,2006,12(14):4147-4153.

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