信号传导和转录激活因子3调控肝癌侵袭转移的研究进展

苟泽鹏; 王德盛; 周亮; 祝普利; 张勇; 孙伟

信号传导和转录激活因子3调控肝癌侵袭转移的研究进展

第四军医大学西京医院肝胆胰脾外科

基金项目:

国家自然科学基金(30872480)；

详细信息

中图分类号: R735.7
计量
- 文章访问数: 3412
- HTML全文浏览量: 9
- PDF下载量: 716
- 被引次数: 0
出版历程
- 出版日期: 2012-04-20

The research progress of STAT3 on the regulation of hepatocellular carcinoma invasion and metastasis

Research funding:

摘要

摘要: 信号传导和转录激活因子(STAT3)是一种信号转导蛋白和转录激活物,可被多种细胞因子激活。被活化的STAT3能转录并激活下游靶基因,引起一系列细胞相关因子的异常表达,与多种恶性肿瘤的发生、发展和侵袭转移关系密切。STAT3在肝癌的发生和发展中同样起着非常重要的作用。本文就其结构、功能及其与肝癌侵袭、转移的研究进展进行综述。
- STAT3转录因子 /
- 肝肿瘤 /
- 肿瘤侵润 /
- 肿瘤转移
Abstract: STAT3 is a signal transduction protein and transcriptional activator, which can be activated by a variety of cytokines.The activated STAT3 could cause abnormal expression of a series of cell-associated factors by transcripting and activating the downstream target genes.It is closely related with the occurrence, development, invasion and metastasis of multiple malignancies.STAT3 plays a very important role in the occurrence and development of hepatocellular carcinoma.This paper focuses on the STAT3′s structure, function and relation between invasion and metastasis of hepatocellular carcinoma.
- STAT3 transcription factor /
- liver neoplasms /
- neoplasm invasion /
- neoplasm metastasis

HTML全文

参考文献(34)

[1]Zhang X, Yue P, Fletcher S, et al.A novel small-moleculedisrupts Stat3 SH2 domain phosphotyrosine interactions andStat3-dependent tumor processes[J].Biochem Pharma-col, 2010, 79 (10) :1398-1409.

[2]Yuen JW, Poon LS, Chan AS, et al.Activation of STAT3 byspecific Galpha subunits and multiple Gbetagamma dimers[J].Int J Biochem Cell Biol, 2010, 42 (6) :1052-1059.

[3]Dourlat J, Liu WQ, Sancier F, et al.A novel non-phospho-rylated potential antitumoral peptide inhibits STAT3 biologicalactivity[J].Biochimie, 2009, 91 (8) :996-1002.

[4]Alshamsan A, Hamdy S, Samuel J, et al.The induction oftumor apoptosis in B16 melanoma following STAT3 siRNAdelivery with a lipid-substituted polyethylenimine[J].Bio-materials, 2010, 31 (6) :1420-1428.

[5]Thelen A, Scholz A, Benckert C, et al.VEGF-D promotestumor growth and lymphatic spread in a mouse model ofhepatocellular carcinoma[J].Int J Cancer, 2008, 122 (11) :2471-2481.

[6]Jablonska J, Leschner S, Westphal K, et al.Neutrophils re-sponsive to endogenous IFN-beta regulate tumor angiogen-esis and growth in a mouse tumor model[J].J Clin Invest, 2010, 120 (4) :1151-1164.

[7]Krol M, Pawlowski KM, Dolka I, et al.Density of Gr1-posi-tive myeloid precursor cells, p-STAT3 expression and geneexpression pattern in canine mammary cancer metastasis[J].Vet Res Commun, 2011, 35 (7) :409-423.

[8]Xu Q, Briggs J, Park S, et al.Targeting Stat3 blocks bothHIF-1 and VEGF expression induced by multiple oncogenicgrowth signaling pathways[J].Oncogene, 2005, 24 (36) :5552-5560.

[9]Hackl C, Mori A, Moser C, et al.Effect of heat-shock pro-tein-90 (HSP90) inhibition on human hepatocytes and onliver regeneration in experimental models[J].Surgery, 2010, 147 (5) :704-712.

[10]Theruvath TP, Jones JA, Ikonomidis JS.Matrix Metallopro-teinases and Descending Aortic Aneurysms:Parity, Dispari-ty, and Switch[J].J Card Surg, 2011, 191 (2) :133-140.

[11]Bauvois B.New facets of matrix metalloproteinases MMP-2 and MMP-9 as cell surface transducers:Outside-in sig-naling and relationship to tumor progression[J].BiochimBiophys Acta, 2011, 1825 (1) :29-36.

[12]Tekle C, Nygren MK, Chen YW, et al.B7-H3 contributes tothe metastatic capacity of melanoma cells by modulation ofknown metastasis-associated genes[J].Int J Cancer, 2011, 128 (1) :216-226.

[13]Wang T, Niu G, Kortylewski M, et al.Regulation of the in-nate and adaptive immune responses by Stat-3 signaling intumor cells[J].Nat Med, 2004, 10 (1) :48-54.

[14]Grivennikov SI, Karin M.Dangerous liaisons:STAT3 and NF-kappaB collaboration and crosstalk in cancer[J].CytokineGrowth Factor Rev, 2010, 21 (1) :11-19.

[15]Oh HM, Yu CR, Golestaneh N, et al.STAT3 protein pro-motes T-cell survival and inhibits interleukin-2 productionthrough up-regulation of Class O Forkhead transcription fac-tors[J].J Biol Chem, 2011, 286 (35) :30888-30897.

[16]German CL, Sauer BM, Howe CL.The STAT3 beacon:IL-6 recurrently activates STAT3 from endosomal structures[J].Exp Cell Res, 2011, 317 (14) :1955-1969.

[17]Shigekawa M, Takehara T, Kodama T, et al.Involvement ofSTAT3-regulated hepatic soluble factors in attenuation ofstellate cell activity and liver fibrogenesis in mice[J].Bio-chem Biophys Res Commun, 2011, 406 (4) :614-620.

[18]Waris G, Siddiqui A.Interaction between STAT-3 and HNF-3leads to the activation of liver-specific hepatitis B virus enhan-cer 1 function[J].J Virol, 2002, 76 (6) :2721-2729.

[19]Machida K, Cheng KT, Lai CK, et al.Hepatitis C virus trig-gers mitochondrial permeability transition with production ofreactive oxygen species, leading to DNA damage and STAT3activation[J].J Virol, 2006, 80 (14) :7199-7207.

[20]Blindenbacher A, Duong FH, Hunziker L, et al.Expressionof hepatitis c virus proteins inhibits interferon alpha signalingin the liver of transgenic mice[J].Gastroenterology, 2003, 124 (5) :1465-1475.

[21]Koeberlein B, Zur HA, Bektas N, et al.Hepatitis B virus over-expresses suppressor of cytokine signaling-3 (SOCS3) there-by contributing to severity of inflammation in the liver[J].VirusRes, 2010, 148 (1-2) :51-59.

[22]Basu A, Meyer K, Lai KK, et al.Microarray analyses andmolecular profiling of Stat3 signaling pathway induced byhepatitis C virus core protein in human hepatocytes[J].Vi-rology, 2006, 349 (2) :347-358.

[23]Ivanov VN, Ghandhi SA, Zhou H, et al.Radiation responseand regulation of apoptosis induced by a combination ofTRAIL and CHX in cells lacking mitochondrial DNA:a role forNF-kappaB-STAT3-directed gene expression[J].ExpCell Res, 2011, 317 (11) :1548-1566.

[24]Li W, Li JJ, Li GL.Expressions of STAT3, VEGF and C-myc in seminoma and their significance[J].Zhonghua NanKe Xue, 2009, 15 (1) :26-30.

[25]Zhang CH, Xu GL, Jia WD, et al.Activation of STAT3 signalpathway correlates with twist and E-Cadherin expression inhepatocellular carcinoma and their clinical significance[J].JSurg Res, 2010, 166 (1) :236-246.

[26]Pan Q, Wang L, Sun HC, et al.Transcription factor activityprofile of human hepatocellular carcinoma cell lines with dif-ferent metastatic potentials[J].Zhonghua Gan Zang Bing ZaZhi, 2006, 14 (1) :37-40.

[27]Bai L, Yang JC, Ok JH, et al.Simultaneous targeting of Srckinase and receptor tyrosine kinase results in synergistic inhi-bition of renal cell carcinoma proliferation and migration[J].Int J Cancer, 2011, 130 (1) :253-262.

[28]Suzuki M, Sugimoto K, Tanaka J, et al.Up-regulation ofglypican-3 in human hepatocellular carcinoma[J].Antican-cer Res, 2010, 30 (12) :5055-5061.

[29]Nault JC, Fabre M, Couchy G, et al.GNAS-activating mu-tations define a rare subgroup of inflammatory liver tumorscharacterized by STAT3 activation[J].J Hepatol, 2011, 55 (5) :973-979.

[30]Chen J, Li G, Meng H, et al.Upregulation of B7-H1 ex-pression is associated with macrophage infiltration in hepato-cellular carcinomas[J].Cancer Immunol Immunother, 2011, 55 (1) :1094-2003.

[31]Li WC, Ye SL, Sun RX, et al.Inhibition of growth and metasta-sis of human hepatocellular carcinoma by antisense oligonucle-otide targeting signal transducer and activator of transcription 3[J].Clin Cancer Res, 2006, 12 (23) :7140-7148.

[32]Avella DM, Li G, Schell TD, et al.Regression of establishedhepatocellular carcinoma is induced by chemo-immunother-apy in an orthotopic murine model[J].Hepatology, 2011, 53 (3) :1002-1011.

[33]侯静, 唐大年, 许媛, 等.STAT3抑制剂对人原发性肝癌细胞生长的影响[J].中华实验外科杂志, 2010, 27 (12) :1822-1824.

[34]Li F, Fernandez PP, Rajendran P, et al.Diosgenin, a ster-oidal saponin, inhibits STAT3 signaling pathway leading tosuppression of proliferation and chemosensitization of humanhepatocellular carcinoma cells[J].Cancer Lett, 2010, 292 (2) :197-207.

施引文献

资源附件(0)

访问统计