期刊文献+

肿瘤抑制基因DBC2抑制乳腺癌MDA-MB-435S细胞增殖并诱导凋亡 被引量:3

DBC2 negatively regulates the proliferation of breast cancer cells and induces apoptosis
原文传递
导出
摘要 目的观察肿瘤抑癌基因DBC2(deletioninbreastcancer2)的过表达在乳腺癌MDA—MB-435S细胞中的功能。方法野生型DBC2基因的真核表达载体pEBG—DBC2瞬时转染MDA—MB-435S细胞72h,噻唑蓝(MTF)比色法绘制DBC2转染前后MDA—MB-435S细胞生长曲线;流式细胞术检测DBC2的瞬时过表达对MDA—MB-435S细胞周期的影响,TUNEL方法原位检测DBC2的过表达诱导MDA—MB-435S细胞凋亡。结果DBC2基因在MDA—MB-435S细胞中的过表达可显著抑制该细胞的增殖,同时DBC2基因的过表达可诱导该乳腺癌细胞周期的G,期阻滞(64.05%比71.72%)和细胞凋亡(0.09%比5.29%)。TUNEL实验证实DBC2诱导MDA—MB-435S细胞凋亡的百分比为8%。结论DBC2基因体外抑制乳腺癌细胞生长的功能,可能通过细胞周期G,期停滞,以及诱导细胞凋亡等机制实现。 Objective To gain insight into the biological function of DBC2 in MDA-MB-435S breast cancer cell line in vitro. Methods Transient DBC2 over-expression in MDA-MB-435S cell line was generated by lipofectamine2000 transfection. MTT assay was performed to verify the function of growth inhibition of DBC2 over-expression. The effects of transient DBC2 over-expression was checked by flow cytometry. TUNEL was used to evaluate the apoptosis induced by DBC2. Results The over-expression of DBC2 could significantly inhibit the proliferation of MDA-MB-435S cells and the percentage of inhibition was from 25.95% to 36.43%. Transient over-expression of DBC2 could also induce cell cycle G1 arrest (64.05% vs. 71.72%). Moreover, TUNEL assay showed that the percentage of apoptosis was about 8%. Conclusion Transient over-expression of DBC2 in vitro could inhibit the growth of breast cancer cells, possibly through the mechanisms of inducing G1 cell cycle arrest and apoptosis.
出处 《中华实验外科杂志》 CAS CSCD 北大核心 2010年第3期345-347,共3页 Chinese Journal of Experimental Surgery
基金 国家自然科学基金资助项目(30400432)
关键词 乳腺癌 肿瘤抑癌基因 增殖 细胞周期 脱噬作用 Breast carcinoma Tumor-suppressing gene Proliferation Cell cycle Apoptosis
  • 相关文献

参考文献11

  • 1Vogelstein B,Kinzler KW.Cancer genes and the pathways they control.Nat Med,2004,10:789-799.
  • 2Sherr CJ.Principles of tumor suppressor.Cell,2004,116:235-246.
  • 3Hamaguchi M,Wigler MH.DBC2,a tumor suppressor gene involved in breast cancer.Prec Natl Aead Sci USA,2002,99:13647-13652.
  • 4Ohadi M,Totonchi M,Maguire P,et al.Mutation analysis of the DBC2 gone in sporadic and familial breast cancer.Aeta Oncel,2007,46:770-772.
  • 5Ho A,Dowdy SF.Regulation of G1 cell-cycle progression by oneogenes and tumor suppressor genes.Curr Opin Genet Dev,2002,12:47-52.
  • 6Yeshihara T,Collado D,Hamaguchi M.Cyelin D1 down-regulation is essential for DBC2's tumor suppressor function.Biochem Biophys Res Commun,2007,358:1076-1079.
  • 7张波,王国斌,刘科,陈剑英.肿瘤抑制基因DBC2在乳腺癌中的表达和对T47D细胞增殖的抑制作用[J].中华实验外科杂志,2008,25(1):15-17. 被引量:3
  • 8Bostrom P,Soderatrom M,Palokangas T,et al.Analysis of Cyclins B1,D1 and E in breast cancer in relation to tumour grade and other prognostic factors.BMC Res Notes,2009,2:140.
  • 9Freeman SN,Ma Y,Cress WD.RhoBTB2(DBC2)is a mitotic E2F1 target gene with a novel role in apoptosis.J Biol Chem,2008,283:2353-2362.
  • 10Sumara I,Peter M.A Cul3-based E3 ligase regulates mitosis and is required to maintain the spindle assembly checkpoint in human cells.Cell Cycle,2007,6:3004-3010.

二级参考文献10

  • 1陈剑英,张波,王国斌,陈庆勇,陈道达.抑癌基因PTEN在乳腺癌激素耐受细胞中的表达[J].中华实验外科杂志,2005,22(10):1195-1197. 被引量:7
  • 2张波,陈剑英,陈道达,王国斌.Cyelin E影响DNA损伤药物对乳腺癌细胞的治疗敏感性[J].中华实验外科杂志,2007,24(1):9-11. 被引量:5
  • 3Antoniou AC, Easton DF. Models of genetic susceptibility to breast cancer. Oncogene ,2006,25:5898-5905.
  • 4Liebens FP, Carly B, Pastijn A ,et al. Management of BRCA1/2 associated breast cancer: a systematic qualitative review of the state of knowledge in 2006. Eur J Cancer,2007,43:238-257.
  • 5Chen ST, Yu SY, Tsai M, et al. Mutation analysis of the putative tumor suppression gene PTEN/MMAC1 in sporadic breast cancer. Breast Cancer Res Treat, 1999,55:85-89.
  • 6Sherr CJ. Principles of tumor suppressor. Cell ,2004,116:235-246.
  • 7Hamaguchi M, Wigler MH. DBC2, a tumor suppressor gene involved in breast cancer. Proc Natl Acad Sci USA ,2002,99 : 13647-13652.
  • 8Ho A, Dowdy SF. Regulation of G1 cell-cycle progression by oncogenes and tumor suppressor genes. Curr Opin Genet Dev,2002,12: 47 -52.
  • 9Tashiro E,Tsuchiya A,lmoto M. Functions of Cyclin D1 as an oncogene and regulation of Cyclin D1 expression. Cancer Sci,2007,98 : 629-635.
  • 10Henriksson M, Luseher B. Proteins of the Myc network : essential regulators of cell growth and differentiation. Adv Cancer Res, 1996,68: 109-182.

共引文献2

同被引文献20

  • 1刘鹏,刘艳,孙慧.小鼠乳腺癌中p53与bcl-2/bax基因表达的相关性研究[J].中华实验外科杂志,2007,24(2):176-178. 被引量:11
  • 2Bulavin DV,Higashimoto Y,Popoff IJ,et al.Initiation of a G2/Mcheckpoint after ultraviolet radiation requires p38 kinase.Nature,2001,411:102-110.
  • 3Bulavin DV,Demidov ON,Saito S,et al.Amplification of PPM1 D in human tumors abrogates p53 tumor-suppressor activity.Nat Genet,2002,31:210-215.
  • 4Li J,Yang Y,Peng Y,et al.Oncogenic properties of PPM1 D located within a breast cancer amplification epicenter at 17q23.Nat Genet,2002,31:133-134.
  • 5Yu E,Ahn YS,Jang SJ,et al.Overexpression of the wip1 gene abrogates the p38 MAPK/p53/Wip1 pathway and silences p16 expression in human breast cancers.Breast Cancer Res Treat,2007,101:269-278.
  • 6Fuku T,Semba S,Yutori H,et al.Increased wild-type p53-induced phosphatase 1 (Wip1 or PPM1 D) expression correlated with downregulation of checkpoint kinase 2 in human gastric carcinoma.Pathol Int,2007,57:566-571.
  • 7Bulavia DV , Demidov ON , Salto S, et al. Amp|ificatiou of PPM1 D in human tumors abrogates p53 tumor-suppressor activity[J]. Nat Genet, 2002, 31 (2) :210 -215.
  • 8Li J, Yang Y, Peng Y, et PPM! D located within a breast at 17q23 [ J ]. Nat Goner, 134. al. Oncogenic properties of cancer amplification epicenter 2002, 31 (2) : 133 -134.
  • 9Le Guezennec X, Bulavin DV. WIP 1 phosphatase at the cross- roads of cancer and aging [ J ] . Trends Biochem Sci , 2010 , 35(2) :109-114.
  • 10Yu E, Ahn YS, Jang S J, et al. Overexpression of the wipl gene abrogates the p38 MAPK/p53 / Wip 1 pathway and silences p 16 expression in human breast cancers [ J ]. Breast Cancer Res Treat, 2007, 101 (3) :269 -278.

引证文献3

二级引证文献16

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