|本期目录/Table of Contents|

[1]李 杨,齐建利,赵立平,等.xCT影响肝癌细胞转移的作用机制研究[J].天津医科大学学报,2014,20(02):93-097.
　LI Yang,QI Jian-li,ZHAO Li-ping,et al.Molecular mechanism of metastasis in hepatocellular carcinoma inhibited by xCT[J].Journal of Tianjin Medical University,2014,20(02):93-097.
点击复制

xCT影响肝癌细胞转移的作用机制研究(PDF)
分享到：

《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
20卷
期数:
2014年02期
页码:
93-097
栏目:
基础医学
出版日期:
2014-03-20

文章信息/Info

Title:
Molecular mechanism of metastasis in hepatocellular carcinoma inhibited by xCT
文章编号:
1006-8147(2014)02-0093-05
作者:
李 杨1; 齐建利1; 赵立平2; 郑雪婷1; 乔海晅1
（天津医科大学 1. 生物医学工程学院 ; 2. 康复与运动医学系，天津300070）
Author(s):
  LI Yang1; QI Jian-li1; ZHAO Li-ping2; ZHENG xue-ting1; QIAO Hai-xuan1
（1.School of Biomedical Engineering;2. Department of Rehabilitation and Sports Medicine, Tianjin Medical University, Tianjin 300070, China）
关键词:
xCT; 肝癌细胞; 自噬; 上皮间质化; 转移
Keywords:
xCT; hepatocellular carcinoma; autophagy; EMT; metastasis
分类号:
R735.7
DOI:
-
文献标志码:
A
摘要:
 目的：探讨人类肝细胞癌中xCT（氨基酸转运系统system x-c的功能性亚基）的表达对于自噬、EMT(上皮细胞间质化)和肿瘤细胞转移的影响。方法：用Western Blot 和RT-PCR方法检测肿瘤细胞在xCT抑制剂SASP(柳氮磺胺毗啶)的作用下，其自噬和EMT过程相关基因的表达水平的改变。伤口愈合实验和Transwell分析xCT在受到抑制后，肿瘤细胞迁移能力的改变。结果：SASP处理过的97H人类高转移肝癌细胞与对照组相比，自噬相关蛋白LC3和Beclin1表达升高，EMT的标志物E-cadherin表达升高，Vimentin的表达降低，参与EMT过程的重要转录因子Snail表达降低。结论：抑制xCT的表达可以使人类高转移肝癌细胞发生自噬，降低转录因子Snail的表达，从而减弱EMT过程的发生并降低人类高转移肝癌细胞的转移能力。
Abstract:
Objective：To discuss the influence of xCT expression on EMT(epithelial-mesenchymal transition) and tumor matastasis in Hepatocellular carcinoma. Methods：Western Blot and RT-PCR were used to detect the expression levels of autophagy and EMT related gene after treated with sulfasalazine (SASP), an inhibitor of xCT activity. Wound healing assay and transwell assay were performed to evaluate the disruption effect of xCT on cell motility. Results：The expression levels of autophagy related protein LC3 and Beclin1 were elevated in SASP treated 97H cells compared with in control 97H cells. E-cadherin was upregulated whereas Vimentin was downregulated when xCT was deficient. Both E-cadherin and Vinmentin were markers of EMT process. Conclusion： xCT disruption can activate autophagy and attenuate EMT, and eventually suppress cell migration.

参考文献/References:

 [1]Liu L, Zhu X D, Wang W Q, et al. Activation of beta-catenin by hypoxia in hepatocellular carcinoma contributes to enhanced metastatic potential and poor prognosis[J]. Clin Cancer Res，2010，16（10）:2740
[2]Chaffer C L, Weinberg R A. A perspective on cancer cell metastasis[J]. Science，2011，331（6024）:1559
[3]Coghlin C, Murray G I. Current and emerging concepts in tumour metastasis[J]. J Pathol，2010，222（1）:1
[4] Klein C A. Cancer: the metastasis cascade[J]. Science，2008，321（5897）:1785
[5] Ledford H. Cancer theory faces doubts[J]. Nature，2011，472（7343）:273
[6]Thiery J P, Acloque H, Huang R Y, et al. Epithelial-mesenchymal transitions in development and disease[J]. Cell，2009，139（7343）:871
[7]Reiman J M, Knutson K L, Radisky D C.Immune promotion of epithelial mesenchymal transition and generation of breast cancer stem cells[J].Cancer Res，2010，70（8）:3005
[8]Bannai S, Ishii T. Transport of cystine and cysteine and cell growth in cultured human diploid fibroblasts: effect of glutamate and homocysteate[J]. J Cell Physiol，1982，112（2）:265
[9]Sato H, Shiiya A, Kimata M, et al. Redox imbalance in cystine/glutamate transporter-deficient mice[J]. J Biol Chem，2005，280（45）:37423
[10]Huang Y, Dai Z, Barbacioru C, et al. Cystine-glutamate transporter SLC7A11 in cancer chemosensitivity and chemoresis tance[J]. Cancer Res，2005，65（16）:7446 [
[11]Calvert P, Yao K S, Hamilton T C, et al. Clinical studies of reversal of drug resistance based on glutathione[J]. Chem Biol Interact，1998，111(2):213
[12]Goto S, Yoshida K, Morikawa T, et al. Augmentation of transport for cisplatin-glutathione adduct in cisplatin-resistant cancer cells[J]. Cancer Res，1995，55（19）:4297 [13]Ruth S, Zvulun E. Regulation of autophagy by ROS:physiology and pathology[J].Cell，2011，36(1):30
[14]Chen R S, Song Y M, Zhou Z Y, et al. Disruption of xCT inhibits cancer cell metastasis via the caveolin-1/ b-catenin pathway[J]. Oncogene，2009，28（4）: 599
[15]Christensen H N. Role of amino acid transport and countertransport in nutrition and metabolism[J]. Physiol Rev，1990，70（1）: 43
[16]Chillaron J, Roca R, Valencia A, et al. Heteromeric amino acid transporters: biochemistry, genetics, and physiology[J]. Am J Physiol Renal Physiol，2001，281（6）:995 [17]Reddy N M, Kleeberger S R, Bream J H, et al. Genetic disruption of the Nrf2 compromises cell-cycle progression by impairing GSH-induced redox signaling[J]. Oncogene，2008，27(44): 5821
[18]Seiler A, Schneider M, Förster H, et al. Glutathione peroxidase 4 senses and translates oxidative stress into 12/15-lipoxygenase dependent-and AIF-mediated cell death[J]. Cell Metab，2008，8(3): 237
[19]Guo W, Zhao Y, Zhang Z, et al. Disruption of xCT inhibits cell growth via the ROS/autophagy pathway in hepatocellular carcinoma[J]. Cancer Letters，2011，312(1): 55
[20]Lv Q, Wang W, Xue J, et al. DEDD Interacts with PI3KC3 to Activate Autophagy and Attenuate Epithelial–Mesenchymal Transition in Human Breast Cancer[J]. Cancer Res，2012，72(13): 3238

相似文献/References:

备注/Memo

备注/Memo:
基金项目 天津市高等学校科技发展基金计划项目（20070908）
作者简介 李杨 （1988-），男，硕士在读，研究方向：细胞生物学； 通信作者：乔海晅， qiaohaixuan@aliyun.com。
更新日期/Last Update: 2014-03-30