期刊文献+

Zebularine联合丁酸钠对结肠癌细胞系LOVO增殖、凋亡以及P16基因表达的影响 被引量:1

Effects of Zebularine and sodium butyrate on cell growth,apoptosis and expression of P16 mRNA in human colon cancer cell line LOVO
暂未订购
导出
摘要 目的探讨Zebularine和丁酸钠对结肠癌LOVO细胞增殖、凋亡及P16基因表达的影响。方法培养人结肠癌细胞系LOVO,分为4组:阴性对照组、Zebularine组、丁酸钠组、Zebularine+丁酸钠组。四甲基偶氮唑蓝(MTT)法检测细胞处理24 h、48 h、72 h后的增殖状况,Annexin V-FITC/PI双染法检测细胞凋亡,逆转录聚合酶链反应(RT-PCR)检测P16基因的表达。结果 Zebula-rine组和丁酸钠组LOVO细胞的抑制率和凋亡率与对照组相比显著增高,Zebularine+丁酸钠组细胞抑制率和凋亡率均显著高于单独用药组(P<0.05);Zebularine组和丁酸钠组P16 mRNA相对表达量显著高于对照组(P<0.05),Zebularine+丁酸钠组P16 mRNA相对表达量显著高于各单独用药组和对照组(P<0.05)。结论与单独用药相比,Zebularine联合丁酸钠可以明显促进P16 mRNA的表达,抑制结肠癌细胞生长。 Objective To investigate the effect of Zebularine and sodium butyrate on cell growth, apoptosis and expression of P16 mRNA in human colon cancer cell line LOVO. Methods Human colon cancer cell lines LOVO were cultured and divided into Zebularine group, sodium butyrate group, Zebularine + sodium butyrate group and control group. The cell growth rate was detected by MTT assay after 24 h, 48 h, 72 h of culture. The cell apoptosis was ana- lyzed by Annexin V-FITC/PI double staining. The expression of P16 mRNA was determined by reverse transcriptase pol- ymerase chain reaction (RT-PCR). Results The cell growth inhibition rate and cell apoptosis rate significantly in- creased in Zebularine group and sodium butyrate group (P 〈 0.05) compared with control group, and the cell growth in- hibition rate and cell apoptosis rate of the Zebularine + sodium butyrate group significantly increased compared with the Zebularine group and sodium butyrate group (P 〈0.05). The relative expression of P16 mRNA of the Zebularine group and sodium butyrate group increased compared with the control, and the relative expression of P16 mRNA of the Zebu- larne + sodium butyrate group significantly increased compared with Zebularine group and sodium butyrate group (P 〈 0.05). Conclusion Compared with separate application of Zebularine or sodium butyrate, joint application could in- crease the expression of P16 mRNA and inhibit the growth of cell line LOVO.
出处 《胃肠病学和肝病学杂志》 CAS 2012年第6期521-524,共4页 Chinese Journal of Gastroenterology and Hepatology
关键词 ZEBULARINE 丁酸钠 P21 凋亡 结肠癌 Zebularine Sodium butyrate P21 Apoptosis Conlon cancer
  • 相关文献

参考文献10

  • 1Cheng JC,Matin CB,Gonzales FA. Inhibition of DNA methylation and reactivation of silenced genes by zebnlarine[J].Journal of the National Cancer Institute,2003,(05):399-409.
  • 2Zhou L,Cheng X,Connolly BA. Zebularine:a novel DNA methylation inhibitor that formss a covalent complex with DNA metbyltransferases[J].Journal of Molecular Biology,2002,(04):591-599.
  • 3Mariadason JM. HDACs and HDAC inhibitors in colon cancer[J].epigenetics,2008,(01):2837.
  • 4Mund C,Beier V,Bewernge P. Array-based analysis of ge nomic DNA methylation patterns of the tumour suppressor gene p16 (INK4A) promoter in colon careinoma cell lines[J].Nucleic Acids Research,2005,(08):e73.doi:10.1093/nar/gni072.
  • 5Egger G,Liang GN,Aparicio A. Epigenetics in human disease and prospects for epigenetic therapy[J].Nature,2004,(6990):457-463.doi:10.1038/nature02625.
  • 6Mossman D,Kim KT,Scou RJ. Demethylation by 5 aza-2'-deoxycyt idine in colorectal cancer cells targets genomic DNA whilst promoter CpG island methylation persists[J].BMC Cancer,2010.366.doi:10.1186/1471-2407-10-366.
  • 7Jutterann R,Li E,Jaenisch R. Toxicity of 5-aza-2-deoxycytidinc to mammalian cells is mediated primarily hy covalent trapping of DNA methyltransferase rather than DNA demethylation[J].Proceedings of the National Academy of Sciences(USA),1994,(25):11797-11801.
  • 8Marquez VE,Barchi JJ,Kelley JA. Zebulanne:a uniqoc molecule for an epigenetically based strategy in cancer chemotherapy.The magic of its chemistry and biology[J].Nucleos Nueleot Nucl,2005,(5-7):305-318.
  • 9Lin HY,Chen CS,Lin SP. Targeting histone deacetylase in cancer therapy[J].Medicinal Research Reviews,2006,(04):397-413.doi:10.1002/med.20056.
  • 10Wu LP,Wang X,Li L. Histone deacetylase inhibitor depsipeptide activates silenced genes through dccreasing bath CpG and H3K9 methylafion on the promoter[J].Molecular and Cellular Biology,2008,(10):3219-3235.doi:10.1128/MCB.01516-07.

同被引文献14

  • 1史健,胡维维,黄小军,周小丽,李广民.自制组织芯片检测宫颈上皮内瘤变中p16蛋白的表达[J].海南医学院学报,2006,12(3):200-203. 被引量:3
  • 2Hagan JP,Croce CM. MicroRNAs in carcinogenesis[J].{H}Cytogenetic and Genome Res,2007,(03):252-259.
  • 3Wang B,Majumder S,Nuovo G. Role of microRNA-155 at early stages of hepatocarcinogenesis induced by choline-deficient and amino acid-defined diet in C57BL/6 mice[J].{H}HEPATOLOGY,2009,(04):1152-1161.
  • 4Staib F,Robles AI,Varticovski L. The p53 tumor suppressor network is a key responder to microenvironmental components of chronic inflammatory stress[J].{H}CANCER RESEARCH,2005,(22):10255-10264.
  • 5Lagos-Quintana M,Rauhut R,Yalcin A. Identification of tissue-specific microRNAs from mouse[J].{H}CURRENT BIOLOGY,2002,(09):735-739.
  • 6Faraoni I,Antonetti FR,Cardone J. miR-155 gene:a typical multifunctional microRNA[J].{H}Biochimica et Biophysica Acta,2009,(06):497-505.
  • 7Thai TH,Calado DP,Casola S. Regulation of the germinal center response by microRNA-155[J].{H}SCIENCE,2007,(5824):604-608.
  • 8Sakano K,Oikawa S,Hasegawa K. Hydroxyurea induces site-specific DNAdamage via formation of hydrogen peroxide and nitric oxide[J].{H}Japanese Journal of Cancer Research,2001,(11):1166-1174.
  • 9Dorsett Y,McBride KM,Jankovic M. MicroRNA-155 suppresses activation-induced cytidine deaminase-mediated myc-igh translocation[J].{H}IMMUNITY,2008,(05):630-638.
  • 10Levati L,Alvino E,Paqani E. Altered expression of selected microRNAs in melanoma:antiproliferative and proapoptotic activity of miRNA-155[J].{H}International Journal of Oncology,2009,(02):393-400.

引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部