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CHOP/GADD153是内质网应激反应特异的转录因子,参与各种细胞活动特别是能量代谢、增殖、分化、凋亡的调节。CHOP在正常情况下表达很低,在内质网应激反应时表达显著升高。CHOP介导的凋亡通路是内质网应激相关凋亡通路中的重要途径。本文综述了CHOP/GADD153介导的细胞凋亡与肿瘤研究的新进展,对于肿瘤的生物治疗具有一定的参考价值。
Abstract:[1]Zha L,Fan L,Sun C,et al.Melatonin sensitizes human hepatoma cells to endoplasmic reticulum stress-induced apoptosis[J].J Pineal Res, 2012,52(3):322.
[2]Oyadomari S,Koizumi A,Takeda K,et al.Targeted disruption of the Chop gene delays endoplasmic reticulum stress-mediated diabetes[J].J din Invest,2002,109(4):525.
[3]Silva RM,Ries V,Oo TF,et al.CHOP/GADD153 is a mediator of apoptotic death in substantia nigra dopamine neurons in an in vim neurotoxin model of parkinsonism[J].J Neurochem,2005,95(4):974.
[4]Ma J,Qiu Y,Yang L,et al.Desipramine induces apoptoeis in rat glioma cells via endoplasmic reticulum stress-dependent CHOP pathway [J].J Neurooncol,2011,101(1):41.
[5]Akatsu Y,Saikawa Y,Kubota T,et al.Predictive value of GADD153, p21 and c-Jun for chemotherapy response in gastric cancer[J].Cancer Sci,2007,98(5):707.
[6]Ron D,Habener JF.CHOP,a novel developmentally regulated nuclear protein that dimerizes with transcription factors C/EBP and LAP and functions as a dominant-negative inhibitor of gene transcription[J]. Genes Dev,1992,6(3):439.
[7]Ubeda M,Wang XZ,Zinszner H,et al.Stress induced binding of the transcriptional factor CHOP to a novel DNA control element[J].Mol Cell Biol,1996,16(4):1479.
[8]Ubeda M,Vallejo M,Habener JF.CHOP enhancement of gene transcription by interactions with Jun/Fos AP-1 complex proteins[J].Mol Cell Biol,1999,19(11):7589.
[9]Schroder M,Kaufman RJ.ER stress and the unfolded protein response [J].Mutat Res,2005.569(1 -2):29.
[10]Shen X,Zhang K,Kaufman RJ.The unfolded protein response-a stress signaling pathway of the endoplasmic reticulum[J].J Chem Neuroanat, 2004,28(1-2):79.
[11]Rao RV,Bredesen DE.Misfolded proteins,endoplasmic reticulum stress and neurodegeneration[J].Curr Opin Cell Biol,2004,16(6): 653.
[12]Boyce M,Yuan J.Cellular response to endoplasmic reticulum stress:a matter of life or death[J].Cell Death Differ,2006,13(3):363.
[13]Kato MA,Finley DJ,Lubitz CC,et al.Selenium decreases thyroid cancer cell growth by increasing expression of GADD153 and GADD34 [J].Nutr Cancer,2010,62(1):66.
[14]Wei MC,ZongWX,Cheng EH,et al.Proapoptotic BAX and BAK:a requisite gateway to mitochondrial dysfunction and death[J].Science, 2001,292(5517):727.
[15]Ohoka N,Yoshii S,Hattori T,et al.TRB3,a novel ER stress-inducible gene,is induced via ATF4-CH0P pathway and is involved in cell death[J].EMBO J,2005,24(6):1243.
[16]Wang XZ,Kuroda M,Sok J,et al.Identification of novel stress-induced genes downstream of chop[J].EMBO J,1998,17(3):3619.
[17]Sok J,Wang XZ,Batchvarova N,et al.CHOP-dependent stress-inducible expression of a novel form of carbonic anhydrase VI[J].Mol Cell Biol,1999,19(1):495.
[18]Hollander MC,Sheikh MS,Yu K,et al.Activation of Gadd34 by diverse apoptotic signals and suppression of its growth inhibitory effects by apoptotic inhibitors[J].Int J Cancer,2001,96(l):22.
[19]Liu L,Chen X,Xie S,et al.Variant 1 of KIAA0101,overexpressed in hepatocellular carcinoma,prevents doxorubicin-induced apoptosis by inhibiting p53 activation[J].Hepatology,2012,56(5):1760.
[20]Withanage K,Nakagawa K,Ikeda M,et al.Expression of RASSF6 in kidney and the implication of RASSF6 and the Hippo pathway in the sorbitol-induced apoptosis in renal proximal tubular epithelial cells[J]. J Biochem,2012,152(1):111.
[21]Chiang PC,Chien CL,Pan SL,et al.Induction of endoplasmic reticulum stress and apoptosis by a marine prostanoid in human hepatocellular carcinoma[J].J Hepatol,2005,43(4):679.
[22]Corazzari M,Lovat PE,Oliverio S,et al.Fenretinide:a p53-inde-pendent way to kill cancer cells[J].Biochem Biophys Res Commun, 2005,331(3):810.
[23]Yeh TC,Chiang PC,Li TK,et al.Cenistein induces apoptosis in human hepatocellular carcinomas via interaction of endoplasmic reticulum stress and mitochondrial insult[J].Biochem Pharmacol,2007,73(6): 782.
[24]Xu Y,Chiu JF,He QY,et al.Tubeimoside-1 exerts cytotoxicity in HeLa cells through mitochondrial dysfunction and endoplasmic reticulum stress pathways[J].J Proteome Res,2009,8(3):1585.
[25]Partacini L,Mancini M,Mazzacurati L,et al.Endoplasmic reticulum stress initiates apoptotic death induced by STI571 inhibition of p210 bcr-abl tyrosine kinase[J].Leuk Res,2004,28(2):191.
[26]Lee AH,Iwakoshi NN,Anderson KC,et al.Proteaaome inhibitors disrupt the unfolded protein response in myeloma cells[J].Proc Natl Acad Sci USA,2003,100(17):9946.
[27]Wu Y,Fabritius M,Ip C.Chemotherapeutic sensitization by endoplasmic reticulum stress[J].Cancer Biol Ther,2009,8(2):146.
[28]Hill DS,Martin S,Armstrong JL et al.Combining the endoplasmic reticulum stress-inducing agents bortezomib and fenretinide as a novel therapeutic strategy for metastatic melanoma[J].Clin Cancer Res, 2009,15(4):1192.
基本信息:
DOI:10.19577/j.cnki.issn10074406.2012.06.019
中图分类号:R96
引用信息:
[1]马健,王浩,苏雪慧,等.抗肿瘤药物作用的新靶点——CHOP/GADD153凋亡通路[J].中国临床药学杂志,2012,21(06):392-394.DOI:10.19577/j.cnki.issn10074406.2012.06.019.
基金信息:
国家自然科学基金(编号:30672442、81071887); 山东省自然科学基金(编号:ZR2011HQ05)
2012-11-25
2012-11-25