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内质网应激与肿瘤
作者:金学英  汪步海 
单位:扬州大学医学院苏北人民医院 肿瘤科, 江苏 扬州 225001
关键词:内质网应激 未折叠蛋白反应 肿瘤 文献综述 
分类号:R730.2
出版年·卷·期(页码):2013·32·第一期(110-114)
摘要:

内质网应激(ERS)是内质网受到多种刺激导致细胞内Ca2+平衡紊乱或内质网中蛋白质堆积引发的反应,ERS中的未折叠蛋白反应(UPR)、内质网超负荷反应(EOR)可能与肿瘤的发生、发展、转移及预后密切相关。本文中作者主要介绍了与肿瘤相关的ERS信号转导通路及相关基因和蛋白的表达与肿瘤的相关性。

参考文献:

[1] PAHL H L.Signal transduction from the endoplasmic reticulum to the cell nucleus[J].Physiol Rev,1999,79:683-701.
[2] FABIO M A.Targeting endoplasmic reticulum signaling pathways in cancer[J].Acta Oncologica,2012,51:822-830.
[3] FELS D R,KOUMENIS C.The PERK/eIF2alpha/ATF4 module of the UPR in hypoxia resistance and tumor growth[J].Cancer Biol Ther,2006,5:723-728.
[4] ADRIENNE M,GORMA N,SANDRA J M,et al.Stress management at the ER:regulators of ER stress-induced apoptosis[J].Pharmacology & Therapeutics,2012,134:306-316.
[5] SHORE G C,PAPA F R,OAKES S A.Signaling cell death from the endoplasmic reticulum stress respons[J].Current Opinion in Cell Biology,2011,23:143-149.
[6] MAIUOLO J,BULOTTA S,VERDERIO C,et al.Selective activation of the transcription factor ATF6 mediatesendoplasmic reticulum proliferation triggered by a membraneprotein[J].Proc Natl Acad Sci USA,2011,108:7832-7837.
[7] EIKE L,PAHL A,PATRICK A.The ER overload response:activation of NF-Κb[J].Biochemical Sciences,1997,2(22):63-67.
[8] SHANSHAN L I,KAUFMAN R J.Stress signaling from the lumen of the endoplasmic reticulum:coordination of gene transcriptional and translational controls[J].Genes Dev,1999,13(10):1211-1233.
[9] CHANA S,HEA F F,WANG H.Calcium entry via TRPC6 mediates albumin overload-induced endoplasmic reticulum stress and apoptosis in podocytes[J].Cell Calcium,2011,50:523-529.
[10] BALKWILLl F,MANTOVANI A.Inflammation and cancer:back to Virchow?[J].Lancet,2001,357(9255):539-545.
[11] HOUGHTON J,STOICOV C,NOMURA S,et al.Gastric cancer originating from bone marrow-derived cells[J].Science,2004,306(5701):1568-1571.
[12] MEURMAN J H.Infectious and dietary risk factors of oral cancer[J].Oral Oncol,2010,46(6):411-413.
[13] SANVAL A J,YOON S K,LENCIONI R.The etiology of hepatocellular carcinoma and consequences for treatment[J].Oncologist,2010,15:14-22.
[14] LI X M,ZHANG K Z,LI Z H.Unfolded protein response in cancer:the physician's perspective[J].J Hematol Oncol,2011,4:8.
[15] GOODALL J C,WU C,ZHANG Y,et al.Endoplasmic reticulum stress-induced transcription factor,CHOP,is crucial for dendritic cell IL-23 expression[J].Proc Natl Acad Sci USA,2010,107(41):17698-17703.
[16] MADONNA G,ULLMAN C D,GENTILCORE G,et al.NF-κB as potential target in the treatment of melanoma[J].J Transl Med,2012,10:53.
[17] DEEB D,GAO X,LIU Y,et al.Synthetic triterpenoid CDDO preventsthe progression and metastasis of prostate cancer in TRAMP miceby inhibiting survival signaling[J].Carcinogenesis,2011,32(5):757-764.
[18] LI C Z,XU J M,LI F G,et al.Unfolded protein response signaling and MAP kinase pathways underlie pathogenesis of arsenic-induced cutaneous inflammation[J].Cancer Prevention Research,2011,4(12):2101-2109.
[19] FUJIWARA J,SOWA Y,HORINAKA M,et al.The anti-obesity drug orlistat promotes sensitivity to TRAIL by two different pathways in hormone-refractory prostate cancer cells[J].Int J Oncol,2012,40(5):1483-1491.
[20] KUROKAWA M,KORNBLUTH S.Caspases and kinases in a death grip[J].Cell,2009,138:838-854.
[21] HITOMI J,KATAYAMA T,EGUCHI Y,et al.Involvement of caspase-4 in endoplasmic reticulumstress-induced apoptosis and Abeta-induced cell death[J].J Cell Biol,2004,165:347-356.
[22] WU L F,WEI B L,GUO Y T,et al.Apoptosis induced by adenosine involves endoplasmic reticulum stress in EC109 cells[J].Int J Mol Med,2012,10:3892.
[23] SUZUKI A,SHIRAKI K.Tumor cell/dead or alive0:caspase and surviving regulate cell death,cell cycle and cell survival[J].Histol Histopathol,2001,16(2):583-593.
[24] HOFFMANN R,von SCHWARZENBERG K.Helenalin by passes Bcl-2-mediated cell death resistance by inhibiting NF-kappa B and promoting reactive oxygen species generation[J].Biochemical Pharmacology,2011,82(5):453-463.
[25] WANG Y,ALAM G N,NING Y.The unfolded protein response induces the angiogenic switch in human tumor cells through the PERK/ATF4 pathway[J].Cancer,2012,72(20):5396-406.
[26] GHOSH R,LIPSON K L.Transcriptional regulation of VEGF-A by the unfolded protein response pathway[J].PLoS One,2010,5(3):e9575.
[27] PEREIRA E R,LIAO N,NEALE G A,et al.Transcriptional and post-transcriptional regulation of proangiogenic factors by the unfolded protein response[J].Plosone,2010,5(9):12-21.
[28] AUF G,JABOUILLE A,GUERUT S,et al.Inositol-requiring enzyme 1α is a key regulator of angiogenesis and invasion in malignant glioma[J].Pnas,2010,107(35):15553-15558.
[29] MANU K A,SHANMUGAM M K,RAMACHANDRAN L.First evidence that γ-tocotrienol inhibits the growth of human gastric cancer and chemosensitizes it to capecitabine in a xenograft mouse model through the modulation of NF-κB pathway[J].2012,15,18(8):2220-2229.
[30] KIMATA Y,KOHNO K.Endoplasmic reticulum stress-sensing mechanisms inyeast and mammalian cells[J].Curr Opin Cell Biol,2011,23:135-142.
[31] FASANO E,SERINI S,PICCIONI E,et al.DHA induces apoptosis by altering the expression and cellular location of GRP78 in colon cancer cell lines[J].Biochim Biophvs Acta,2012,1822(11):1762-1772.
[32] MARTIN S,HILL D S,PATON J C,et al.Targeting GRP78 to enhance melanoma cell death[J].Pigment Cell Melanoma Res,2010,23(5):675-682.
[33] SCRIVEN P,COULSON S,HAINES R,et al.Activation and clinical significance of the unolded protein response in breast cancer[J].Br J Cancer,2009,101(10):1692-1698.
[34] HUANG K U,KUO K L,CHEN S C,et al.Down-regulation of glucose-regulated protein (GRP) 78 potentiates cytotoxic effect of celecoxib in human urothelial carcinoma cells[J].PLoS One,2012,7(3):e33615.
[35] GORMAN A M,HEALY S J M,JÄGER R,et al.Stress management at the ER:regulators of ER stress-induced apoptosis[J].Pharmacology & Therapeutics,2012,134:306-316.

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