[1]何颖,张竹君.IBP通过上皮间质转化促进结肠癌细胞迁移和侵袭[J].第三军医大学学报,2016,38(11):1281-1285.
 He Ying,Zhang Zhujun.IBP promotes migration and invasion in colon cancer cells via epithelial to mesenchymal transition[J].J Third Mil Med Univ,2016,38(11):1281-1285.
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《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
38卷
期数:
2016年第11期
页码:
1281-1285
栏目:
基础医学
出版日期:
2016-06-15

文章信息/Info

Title:
IBP promotes migration and invasion in colon cancer cells via epithelial to mesenchymal transition
作者:
何颖张竹君
第三军医大学新桥医院超声科;第三军医大学西南医院医学检验系临床微生物及免疫学教研室
Author(s):
He Ying Zhang Zhujun

Department of Ultrasonography, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037; Department of Clinical Microbiology and Immunity, Faculty of Medical Laboratory Sciences, Southwest Hospital, Third Military Medical University, Chongqing, 400038, China

关键词:
干扰素调节因子4结合蛋白结肠癌上皮间质转化迁移侵袭
Keywords:
interferon regulatory factor-4 binding protein colon cancer epithelial-mesenchymal transition migration invasion
分类号:
R341; R730.23; R735.35
文献标志码:
A
摘要:

目的      探讨干扰素调节因子4结合蛋白(interferon regulatory factor-4 binding protein, IBP)能否影响结肠癌细胞上皮间质转化(epithelial to mesenchymal transition, EMT)的发生,观察IBP在肿瘤细胞增殖、迁移和侵袭中作用。      方法      干预结肠癌细胞中IBP的表达,构建IBP过表达的HT-29-IBP细胞株与IBP沉默的HCT116-shIBP细胞株;干预IBP表达后,采用Western blot检测结肠癌细胞EMT相关分子的蛋白表达;Transwell实验检测结肠癌细胞迁移、侵袭能力的改变;MTT实验检测结肠癌细胞增殖能力的改变。      结果      HT-29-IBP细胞中上皮相关分子E-cadherin和ZO-1表达水平降低,间质相关分子Fibronectin表达升高,细胞增殖、迁移和侵袭能力增强(P<0.05); HCT116-shIBP细胞则E-cadherin、ZO-1表达水平升高,Fibronectin及Snail表达降低,细胞增殖、迁移和侵袭能力降低(P<0.05)。      结论      IBP通过调节EMT促进结肠癌细胞增殖、迁移和侵袭。

Abstract:

Objective      To determine the role of interferon regulatory factor-4 binding protein (IBP) in epithelial to mesenchymal transition (EMT), and investigate its effect on the migration and invasion of colon cancer cells.       Methods      Colon cancer HT-29 and HCT116 cells were transfected with pcDNA3.1 (+)-IBP plasmid or infected with recombined shIBP lentivirus, and the stable clones were selected with G418 or puromycin. The expression of IBP and EMT-related molecules was detected in the HT-29-IBP cells and HCT116-shIBP cells by Western blotting. MTT assay was performed to investigate the effect of IBP on the proliferation, and Transwell chamber assay was carried out on the migration and invasion in colon cancer cells.       Results      Over-expression of IBP decreased the expression levels of epithelial markers, E-cadherin and ZO-1, while increased the mesenchymal marker, Fibronectin, and promoted the proliferation, migration and invasion in the HT-29-IBP cells (P<0.05). However, silencing of IBP up-regulated the expression of E-cadherin and ZO-1, but down-regulated the levels of Fibronectin and Snail, and decreased the proliferation, migration and invasion in the HCT116-shIBP cells (P<0.05).       Conclusion       IBP promotes the proliferation, migration and invasion of colon cancer cells through regulating EMT.

参考文献/References:

[1]Torre L A, Bray F, Siegel R L, et al. Global cancer statistics, 2012[J]. CA Cancer J Clin, 2015, 65(2): 87-108. DOI: 10.3322/caac.21262
[2]Thiery J P. Epithelial-mesenchymal transitions in tumour progression[J]. Nat Rev Cancer, 2002, 2(6): 442-454. DOI: 10. 1038/nrc822
[3]Tiwari N, Gheldof A, Tatari M, et al. EMT as the ultimate survival mechanism of cancer cells[J]. Semin Cancer Biol, 2012, 22(3): 194-207. DOI: 10.1016/j.semcancer. 2012.02.013
[4]Bates R C, Goldsmith J D, Bachelder R E, et al. Flt-1- dependent survival characterizes the epithelial-mesenchymal transition of colonic organoids[J]. Curr Biol, 2003, 13(19): 1721-1727.
[5]Gulhati P, Bowen K A, Liu J, et al. mTORC1 and mTORC2 regulate EMT, motility, and metastasis of colorectal cancer via RhoA and Rac1 signaling pathways[J]. Cancer Res, 2011, 71(9): 3246-3256. DOI: 10.1158/0008-5472. CAN-10-4058
[6]Bowen K A, Doan H Q, Zhou B P, et al. PTEN loss induces epithelial--mesenchymal transition in human colon cancer cells[J]. Anticancer Res, 2009, 29(11): 4439-4449.
[7]Mavrakis K J, McKinlay K J, Jones P, et al. DEF6, a novel PH-DH-like domain protein, is an upstream activator of the Rho GTPases Rac1, Cdc42, and RhoA[J]. Exp Cell Res, 2004, 294(2): 335-344. DOI: 10.1016/j.yexcr.2003.12.004
[8]Yilmaz M, Christofori G. EMT, the cytoskeleton, and cancer cell invasion[J]. Cancer Metastasis Rev, 2009, 28(1/2): 15-33. DOI: 10.1007/s10555-008-9169-0
[9]Vega F M, Ridley A J. Rho GTPases in cancer cell biology[J]. FEBS Lett, 2008, 582(14): 2093-2101. DOI: 10.1016/j.febslet.2008.04.039
[10]Becart S, Charvet C, Canonigo-Balancio A J, et al. SLAT regulates Th1 and Th2 inflammatory responses by controlling Ca2+/NFAT signaling[J]. J Clin Invest, 2007, 117(8): 2164-2175. DOI: 10.1172/JCI31640
[11]Fanzo J C, Yang W, Jang S Y, et al. Loss of IRF-4-binding protein leads to the spontaneous development of systemic autoimmunity[J]. J Clin Invest, 2006, 116(3): 703-714. DOI: 10.1172/JCI24096
[12]Zhang Z, Yang M, Chen R, et al. IBP regulates epithelial- to-mesenchymal transition and the motility of breast cancer cells via Rac1, RhoA and Cdc42 signaling pathways[J]. Oncogene, 2014, 33(26): 3374-3382. DOI: 10.1038/onc.2013.337
[13]Zhang Z, Wang Q, Li P, et al. Overexpression of the Interferon regulatory factor 4-binding protein in human colorectal cancer and its clinical significance[J]. Cancer Epidemiol, 2009, 33(2): 130-136.DOI: 10.1016/j.canep.2009.05.004
[14]Li P, Zhang Z, Wang Q, et al. The ectopic expression of IFN regulatory factor 4-binding protein is correlated with the malignant behavior of human breast cancer cells[J]. Int Immunopharmacol, 2009, 9(7/8): 1002-1009. DOI: 10.1016/j.intimp. 2009. 04.008
[15]Chalya P L, McHembe M D, Mabula J B, et al. Clinicopathological patterns and challenges of management of colorectal cancer in a resource-limited setting: a Tanzanian experience[J]. World J Surg Oncol, 2013, 11: 88. DOI: 10.1186/1477-7819-11-88
[16]Gupta S, Lee A, Hu C, et al. Molecular cloning of IBP, a SWAP-70 homologous GEF, which is highly expressed in the immune system[J]. Hum Immunol, 2003, 64(4): 389-401.
[17]Tanaka Y, Bi K, Kitamura R, et al. SWAP-70-like adapter of T cells, an adapter protein that regulates early TCR-initiated signaling in Th2 lineage cells[J]. Immunity, 2003, 18(3): 403-414.
[18]Canonigo-Balancio A J, Fos C, Prod’homme T, et al. SLAT/Def6 plays a critical role in the development of Th17 cell-mediated experimental autoimmune encephalomyelitis[J]. J Immunol, 2009, 183(11): 7259-7267. DOI: 10.4049/jimmunol.0902573
[19]Goudevenou K, Martin P, Yeh Y J, et al. Def6 is required for convergent extension movements during zebrafish gastrulation downstream of Wnt5b signaling[J]. PLoS One, 2011, 6(10): e26548. DOI: 10.1371/journal.pone.0026548
[20]Chen Q, Gupta S, Pernis A B. Regulation of TLR4- mediated signaling by IBP/Def6, a novel activator of Rho GTPases[J]. J Leukoc Biol, 2009, 85(3): 539-543. 10.1189/jlb.0308219
[21]Hotfilder M, Baxendale S, Cross M A, et al. Def-2, -3, -6 and -8, novel mouse genes differentially expressed in the haemopoietic system[J]. Br J Haematol, 1999, 106(2): 335-344.
[22]Shuman-Moss L A, Jensen-Taubman S, Stetler-Stevenson W G. Matrix metalloproteinases: changing roles in tumor progression and metastasis[J]. Am J Pathol, 2012, 181(6): 1895-1899. DOI: 10.1016/j.ajpath.2012.08.044
[23]Arvelo F, Cotte C. Metalloproteinases in tumor progression. Review[J]. Invest Clin, 2006, 47(2): 185-205.

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更新日期/Last Update: 2016-05-29