高级搜索

r-H2AX在不同食管癌株系中的剂量时间效应特点

史鸿云, 祝淑钗, 卢付河, 王玉祥, 苑兰惠, 何丽

史鸿云, 祝淑钗, 卢付河, 王玉祥, 苑兰惠, 何丽. r-H2AX在不同食管癌株系中的剂量时间效应特点[J]. 肿瘤防治研究, 2013, 40(04): 321-326. DOI: 10.3971/j.issn.1000-8578.2013.04.002
引用本文: 史鸿云, 祝淑钗, 卢付河, 王玉祥, 苑兰惠, 何丽. r-H2AX在不同食管癌株系中的剂量时间效应特点[J]. 肿瘤防治研究, 2013, 40(04): 321-326. DOI: 10.3971/j.issn.1000-8578.2013.04.002
SHI Hongyun, ZHU Shuchai, LU Fuhe, WANG Yuxiang, YUAN Lanhui, HE Li. Expression of r-H2AX in Time-effect and Dose-response between Different Esophageal Carcinoma Cell Lines[J]. Cancer Research on Prevention and Treatment, 2013, 40(04): 321-326. DOI: 10.3971/j.issn.1000-8578.2013.04.002
Citation: SHI Hongyun, ZHU Shuchai, LU Fuhe, WANG Yuxiang, YUAN Lanhui, HE Li. Expression of r-H2AX in Time-effect and Dose-response between Different Esophageal Carcinoma Cell Lines[J]. Cancer Research on Prevention and Treatment, 2013, 40(04): 321-326. DOI: 10.3971/j.issn.1000-8578.2013.04.002

r-H2AX在不同食管癌株系中的剂量时间效应特点

基金项目: 国家自然科学基金资助项目(30870743)
详细信息
    作者简介:

    史鸿云(1979-),女,博士在读,主治医师,主要从事食管癌基础与临床研究

    通讯作者:

    祝淑钗,E-mail:sczhu@heinfo.net

  • 中图分类号: R735.1

Expression of r-H2AX in Time-effect and Dose-response between Different Esophageal Carcinoma Cell Lines

  • 摘要: 目的 通过检测不同食管癌株系的r-H2AX时间剂量效应关系,了解r-H2AX的动力学特点。 方法 将食管癌ECA109和TE13两种细胞株分别给予1、2、4和8Gy 的6MV-X线照射,并分别于0.5、1、2、4、8、12、24 h收集细胞提取蛋白,检测r-H2AX时间及剂量效应特点。 结果 (1) ECA109细胞和TE13细胞随着放疗剂量的增加,r-H2AX表达量第一次最高点出现的时间逐渐提前。(2) ECA109细胞接受低剂量照射后,r-H2AX在24 h内能够恢复到放疗前的水平,且剂量越低恢复越快;TE13细胞接受1、2、4和8Gy照射后24 h内r-H2AX均不能恢复到放疗前水平。(3)在0.5、1、2 h这3个时间点,随着放疗剂量的增加,r-H2AX的表达量并不都是逐渐增加。结论 TE13细胞较ECA109细胞敏感,照射后r-H2AX更难恢复到正常水平。

     

    Abstract: Objective To investigate the time-effect and dose-effect of r-H2AX in different esophageal carcinoma lines after irradiation. Methods The dose-response(1,2,4,8Gy) and time-effect of r-H2AX in different esophageal carcinoma lines after irradiation were studied and compared by Western blot.Two cell lines of esophageal carcinoma (ECA109 and TE13) were radiated by 6MV-X ray of (1, 2, 4 and 8Gy) The cells and extracted proteins at 0.5, 1, 2, 4, 8, 12 and 24 h were collected and to study the dose-response and time-effect relationship of r-H2AX. Results (1) The first peak of r-H2AX expression gradually appeared in advance with the increasing radiation dose of ECA109 cells and TE13 cells. (2) r-H2AX within 24 hours recovered to the level before radiotherapy after low-dose irradiation in ECA109, The level recovered faster if the dose of radiation is lower; r-H2AX can not be recovered to the level before radiotherapy after irradiation of 1,2,4 and 8Gy within 24 h in TE13. (3) At 0.5, 1 and 2 h,the expression of r-H2AX in ECA109 and TE13 cells didn't increase with the increase in radiation dose. Conclusion The level of r-H2AX is more difficult to return to normal levels in TE13 cell line than in ECA109 cell line after irradiation which shows that TE13 is more sensitive to irradiation.

     

  • [1] Fisehle W,Wang Y,Allis CD. Histone and chromatineross-talk[J]. Curr Opin Cell Biol, 2003,15 (2): 172-83.
    [2] Celeste A, Fernandez-Capetillo O, Kruhlak MJ, et al. Histone H2AX phosphorylation is dispensable for the initial recognition of DNA breaks [J]. Nat Cell Biol, 2003,5 (7):675-9.
    [3] Fernandez-Capetillo O, Lee A, Nussenzweig M, et al.H2AX: the histone guardian of the genome[J]. DNA Repair (Amst), 2004,3 (8-9): 959-67.
    [4] Bonner WM, Redon CE, Dickey JS, et al. GammaH2AX and cancer[J].Nat Rev Cancer, 2008,8 (12) :957-67.
    [5] Rogakou EP, Pilch DR, Orr AH, et al. DNA double-stranded breaks induce histone H2AX phosphorylation on serine 139 [J] . J Biol Chem, 1998,273 (10):5858-68.
    [6] Giunta S, Belotserkovskaya R, Jackson SP. DNA damage signaling in response to double-strand breaks during mitosis [J]. J Cell Biol, 2010,190 (2) :197-207.
    [7] Suit H. The Gray Lecture 2001: coming technical advances in radiation oncology [J]. Int J Radiat Oncol Biol Phys,2002,53(4) :798-809.
    [8] Vokes EE, Haraf DJ, Brockstein BE, et al. Paclitaxel, 5-fluorouracil, hydroxyurea, and concomitant radiation therapy for poor-prognosis head and neck cancer[J]. Semin Radiat Oncol,1999,9 (2 Suppl 1 ):70-6.
    [9] Milas L, Mason KA, Liao Z, et al. Chemoradiotherapy: emerging treatment improvement strategies [J]. Head Neck ,2003,25(2):152-67.
    [10] Weichselbaum RR. Growth factors alter the therapeutic ratio in radiotherapy[J].Cancer J Sci Am, 1995,1 (1): 28-9.
    [11] Chmura SJ, Gupta N, Advani SJ, et al. Prospects for viral-based strategies enhancing the anti-tumor effects of ionizing radiation [J]. Semin Radiat Oncol, 2001,11(4) :338-45.
    [12] Olive PL, Banáth JP. Phosphorylation of histone H2AX as a measure of radiosensitivity [J]. Int J Radiat Oncol Biol Phys,2004,58 (2):331-5.
    [13] Kanaar R, Hoeijmakers JH, van Gent DC. Molecular mech-anisms of DNA double-strand break repair [J]. Trends Cell Biol ,1998,8 (12):483-9.
    [14] Dasika GK, Lin SC, Zhao S, et al. DNA damage-induced cell cycle checkpoints and DNA strand break repair in development and tumorigenesis [J]. Oncogene, 1999,18 (55) 7883-99.
    [15] Green CM, Almouzni G. When repair meets chromatin. First in series on chromatin dynamics[J]. EMBO Rep, 2002,3 (1):28-33.
    [16] Smerdon MJ, Conconi A. Modulation of DNA damage and DNA repair in chromatin [J]. Prog Nucleic Acid Res Mol Biol,1999,62:227-55.
    [17] MacPhail SH, Ban th JP, Yu Y, et al. Cell cycle-dependent expression of phosphorylated histone H2AX: reduced expression in unirradiated but not X-irradiated G1-phase cells [J]. Radiat Res, 2003,159 (6): 759-67.
    [18] Taneja N, Davis M, Choy JS, et al. Histone H2AX phosphorylation as a predictor of radiosensitivity and target for radiotherapy [J]. J Biol Chem, 2004,279(3): 2273-80.
    [19] Banāth JP, MacPhail SH, Olive PL. Radiation sensitivity, H2AX phosphorylation, and kinetics of repair of DNA strand breaks in irradiated cervical cancer cell lines[J]. Cancer Res,2004,64(19):7144-9.
    [20] Kühne M, Riballo E, Rief N, et al. A double-strand break repair defect in ATM-deficient cells contributes to radiosensitivity [J] .Cancer Res, 2004,64 (2): 500-8.
    [21] Mahrhofer H, Burger S, Oppitz U, et al. Radiation induced DNA damage and damage repair in human tumor and fibroblast cell lines assessed by histone H2AX phosphorylation[J]. Int J Radiat Oncol Biol Phys, 2006,64 (2) :573-80.
    [22] Paull TT, Rogakou EP, Yamazaki V, et al. A critical role for histone H2AX in recruitment of repair factors to nuclear foci after DNA damage [J].Curr Biol, 2000,10 (15):886-95.
计量
  • 文章访问数:  2192
  • HTML全文浏览量:  15
  • PDF下载量:  302
  • 被引次数: 0
出版历程
  • 收稿日期:  2012-05-30
  • 修回日期:  2012-09-04
  • 刊出日期:  2013-04-24

目录

    /

    返回文章
    返回
    x 关闭 永久关闭