MAFG:癌症治疗潜在靶点-CSCIED科技核心评价数据库-手机版

MAFG:癌症治疗潜在靶点

MAFG: A promising target for cancer therapy

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刊名	生命的化学
年，卷(期)	2018, 38(05)
作者	杨玉容1,2李子涵1夏磊1,2张素君2周志刚3涂剑1,
作者单位	1.南华大学药学院2.南华大学医学研究中心3.南华大学附属第一医院麻醉科
摘要	碱性亮氨酸拉链家族转录因子V-Maf鸟类肌筋膜纤维肉瘤癌基因同源物(musculoaponeurotic fibrosarcoma, MAF) G在人正常组织表达较低,但在黑色素瘤、结肠直肠癌、肺癌和胆管细胞型肝癌等癌组织表达显著增强。通过网上收集肝细胞型肝癌(hepatocellular carcinoma, HCC)临床样本的公共数据库,发现MAFG在癌组织的表达显著高于癌旁组织,而且高表达MAFG的HCC患者预后差于低/中表达者。以上均提示MAFG是又一潜在的促癌因子。本文就MAFG在癌症中高表达的作用及其可能机制作一综述。
Abstract	Recent studies have found that the expression of V-Maf avian musculoaponeurotic fibrosarcoma oncogene homolog G, abbreviated to MAFG, was low in human normal tissues, while it was significantly higher in many cancers such as malignant melanoma, carcinoma of colon and rectum, lung cancer and cholangiocarcinoma, and so on. We have collected the clinical samples of hepatocellular carcinoma (HCC) from public database and found that MAFG expression was significantly higher in cancer tissues than that in paracancerous tissues. Furthermore, the prognosis of HCC patients with high expression of MAFG was worse than those with low/moderate expression. All above suggest that MAFG is another potential cancer promoter. This article has reviewed the role and possible mechanisms of MAFG high expressed in the cancer.
关键词	MAFG;癌症治疗;潜在靶点;
KeyWord	MAFG;cancer therapy;promising target
基金项目
页码	689-694

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相关文献

[1] Blank V, Knoll JH, Andrews NC. Molecular characterization and localization of the human MAFG gene. Genomics, 1997, 44(1): 147- 149

[2] Anand D, Agrawal SA, Siddam AD, et al. An integrative approach to analyze microarray datasets for prioritization of genes relevant to lens biology and disease. Genomics Data, 2015, 5: 223- 227

[3] Agrawal SA, Anand D, Siddam AD, et al. Compound mouse mutants of bZIP transcription factors Mafg and Mafk reveal a regulatory network of non- crystallin genes associated with cataract. Human Genetics, 2015, 134(7): 717- 735

[4] Yamazaki H, Katsuoka F, Motohashi H, et al. Embryonic lethality and fetal liver apoptosis in mice lacking all three small Maf proteins. Mol Cell Biol, 2012, 32(4): 808- 816

[5] Katsuoka F, Motohashi H, Engel JD, et al. Nrf2 transcriptionally activates the mafG gene through an antioxidant response element. J Biol Chem, 2005, 280(6): 4483- 4490

[6] Caggiano R, Cattaneo F, Moltedo O, et al. miR- 128 is implicated in stress responses by targeting mafg in skeletal muscle cells. Oxid Med Cell Longev, 2017, 2017: 9308310

[7] Motohashi H, Katsuoka F, Miyoshi C, et al. MafG sumoylation is required for active transcriptional repression. Mol Cell Biol, 2006, 26(12): 4652- 4663

[8] Fang M, Hutchinson L, Deng A, et al. Common BRAF(V600E)- directed pathway mediates widespread epigenetic silencing in colorectal cancer and melanoma. Proc Natl Acad Sci USA, 2016, 113(5): 1250- 1255

[9] Motohashi H, Fujita R, Takayama M, et al. Molecular determinants for small Maf protein control of platelet production. Mol Cell Biol, 2011, 31(1): 151- 162

[10] Fang M, Ou J, Hutchinson L, et al. The BRAF oncoprotein functions through the transcriptional repressor MAFG to mediate the CpG island methylator phenotype. Mol Cell, 2014, 55(6): 904- 915

[11] Wang X, Chorley BN, Pittman GS, et al. Genetic variation and antioxidant response gene expression in the bronchial airway epithelium of smokers at risk for lung cancer. PLoS One, 2010, 5(8): e11934

[12] Yang H, Liu T, Wang J, et al. Deregulated methionine adenosyltransferase α1, c- Myc and Maf proteins together promote cholangiocarcinoma growth in mice and humans. Hepatology, 2016, 64(2): 439- 455

[13] Liu T, Yang H, Fan W, et al. MAFG dysregulation in cholestatic liver injury and development of liver cancer. Gastroenterology, 2018, 155(2): 557- 571

[14] Hirotsu Y, Higashi C, Fukutomi T, et al. Transcription factor NF- E2- related factor 1 impairs glucose metabolism in mice. Genes Cells, 2014, 19(8): 650- 665

[15] Yamazaki H, Katsuoka F, Motohashi H, et al. Embryonic lethality and fetal liver apoptosis in mice lacking all three small Maf proteins. Mol Cell Biol, 2012, 32(4): 808- 816

[16] Akira Kobayashi, Moonil Kang, Hiromi Okawa, et al. Oxidative stress sensor keap1 functions as an adaptor for Cul3- Based E3 Ligase to regulate proteasomal degradation of Nrf2. Mol Cell Biol, 2004, 24(16): 7130- 7139

[17] Li L, Dong H, Song E, et al. Nrf2/ARE pathway activation, HO- 1 and NQO1 induction by polychlorinated biphenyl quinone is associated with reactive oxygen species and PI3K/AKT signaling. Chem Biol Interact, 2014, 209: 56- 67

[18] Kensler TW, Wakabayashi N. Nrf2: friend or foe for chemoprevention? Carcinogenesis, 2010, 31(1): 90- 99

[19] Motohashi H, Katsuoka F, Engel JD, et al. Small Maf proteins serve as transcriptional cofactors for keratinocyte differentiation in the Keap1- Nrf2 regulatory pathway. Proc Natl Acad Sci USA, 2004, 101(17): 6379- 6384

[20] Kundu JK, Surh YJ. Nrf2- Keap1 signaling as a potential target for chemoprevention of inflammation- associated carcinogenesis. Pharm Res, 2010, 27(6): 999- 1013

[21] Yang YM, Roh YS, Seki E. MAFG, A novel target of fkr that regulates bile acidomeostasis. Gastroenterology, 2015, 149(7): 1981- 1983

[22] Dhakshinamoorthy S, Jaiswal AK. Small maf (MafG and MafK) proteins negatively regulate antioxidant response element- mediated expression and antioxidant induction of the NAD(P)H: Quinone oxidoreductase1 gene. J Biol Chem, 2000, 275(51): 40134- 40141

[23] Yang H, Ko K, Xia M, et al. Induction of avian musculoaponeurotic fibrosarcoma proteins by toxic bile acid inhibits expression of glutathione synthetic enzymes and contributes to cholestatic liver injury in mice. Hepatology, 2010, 51(4): 1291- 1301

[24] Kimura M, Yamamoto T, Zhang J, et al. Molecular basis distinguishing the DNA binding profile of Nrf2- Maf heterodimer from that of Maf homodimer. J Biol Chem, 2015, 290(17): 10644

[25] Sun J, Brand M, Zenke Y, et al. Heme regulates the dynamic exchange of Bach1 and NF- E2- related factors in the Maf transcription factor network. Proc Natl Acad Sci USA, 2004, 101(6): 1461- 1466

[26] Khaleghian M, Shakoori A, Razavi AE, et al. Relationship of amplification and expression of the C- MYC gene with survival among gastric cancer patients. Asian Pac J Cancer Prev, 2015, 16(16): 7061- 7069

[27] Higgs MR, Lerat H, Pawlotsky JM. Hepatitis C virus- induced activation of β- catenin promotes c- Myc expression and a cascade of pro- carcinogenic events. Oncotarget, 2013, 32(39): 4683- 4693

[28] Fan W, Yang H, Liu T, et al. Prohibitin 1 suppresses liver cancers tumorigenesis in mice and human hepatocellular and cholangiocarcinoma cells. Hepatology, 2017, 65(4): 1249- 1266

[29] Ko KS, Tomasi ML, Iglesias- Ara A, et al. Liver- specific deletion of prohibitin 1 results in spontaneous liver injury, fibrosis, and hepatocellular carcinoma in mice. Hepatology, 2010, 52(6): 2096- 2108

[30] Pa?eda C, Gorospe I, Herrera B, et al. Liver cell proliferation requires methionine adenosyltransferase 2A mRNA up- regulation. Hepatology, 2002, 35(6): 1381- 1391

[31] Tomasi ML, Ryoo M, Ramani K, et al. Methionine adenosyltransferase α2 sumoylation positively regulate Bcl- 2 expression in human colon and liver cancer cells. Oncotarget, 2015, 6(35): 37706- 37723

[32] Schembri F, Sridhar S, Perdomo C, et al. MicroRNAs as modulators of smoking- induced gene expression changes in human airway epithelium. Proc Natl Acad Sci USA, 2009, 106(7): 2319- 2324

[33] Vera O, Jimenez J, Pernia O, et al. DNA Methylation of miR- 7 is a mechanism involved in platinum response through mafg overexpression in cancer cells. Theranostics, 2017, 7(17): 4118- 4134

[34] Chewchuk S, Boorman T, Edwardson D, et al. Bile acids increase doxorubicin sensitivity in abcc1- expressing tumour cells. Sci Rep, 2018, 8(1): 5413

[35] Zhang Y, LaCerte C, Kansra S, et al. Comparative potency of obeticholic acid and natural bile acids on FXR in hepatic and intestinal in vitro cell models. Pharmacol Res Perspect, 2017, 5(6): 1- 10

[36] Namisaki T, Moriya K, Kitade M, et al. Effect of combined farnesoid X receptor agonist and angiotensin II type 1 receptor blocker on hepatic fibrosis. Hepatol Commun, 2017, 1(9): 928- 945

[37] de Aguiar Vallim TQ, Tarling EJ, Ahn H, et al. MAFG is a transcriptional repressor of bile acid synthesis and metabolism. Cell Metab, 2015, 21(2): 298- 311

[38] Guo C, LaCerte C, Edwards JE, et al. Farnesoid X receptor agonists obeticholic acid and chenodeoxycholic acid increase bile acid efflux in sandwich- cultured human hepatocytes: functional evidence and mechanisms. J Pharmacol Exp Ther, 2018, 365(2): 413- 421

[39] Hirotsu Y, Katsuoka F, Funayama R, et al. Nrf2- MafG heterodimers contribute globally to antioxidant and metabolic networks. Nucleic Acids Res, 2012, 40(20): 10228- 10239

[40] Sun X, Ou Z, Chen R, et al. Activation of the p62- Keap1- NRF2 pathway protects against ferroptosis in hepatocellular carcinoma cells. Hepatology, 2016, 63(1): 173- 184

引用本文

杨玉容,李子涵夏磊,张素君周志刚涂剑. MAFG:癌症治疗潜在靶点 [J]. 生命的化学. 2018; 38; (05). 689 - 694.

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