[1] Dai Z, Wu Z, Wang J, et al.Analysis of polyamines in biological samples by HPLC involving pre-column derivatization with o-phtha-laldehyde and N-acetyl-L-cysteine[J].Amino Acids, 2014, 46:1557-1564. [2]He H, Kang B, Jiang DM, et al.Molecular cloning and mRNA expression analysis of ornithine decarboxylase antizyme 2 in ovarian follicles of the Sichuan white goose(Anser cygnoides)[J].Gene, 2014, 545:247-252. [3]王贵鸿, 马容, 康波, 等.多胺跨膜物质转运的机制[J].动物营养学报, 2014, 26:3245-3250. [4]Kruczynski A, Vandenber I, Pillon A, et al.Preclinical activity of F14512, designed to target tumors expressing an active polyamine transport system[J].Invest New Drugs, 2011, 29:9-21. [5]Gerner EW, Meyskens FL Jr.Polyamines and cancer:old molecules, new understanding[J].Nat Rev Cancer, 2004, 4:781-792. [6] Thomas T, Thomas TJ.Polyamine metabolism and cancer[J].Journal of Cellular and Molecular Medicine, 2003, 7:113-126. [7] 易星, 莫远亮, 姜冬梅, 等.多胺的生物学功能及其调控机制[J].动物营养学报, 2014, 26:348-352. [8] Tobias KE, Shor J, Kahana C.c-Myc and Max transregulate the mouse ornithine decarboxylase promoter through interaction with two downstream CACGTG motifs[J].Oncogene, 1995, 11:1721-1727. [9] Shantz LM, Levin VA.Regulation of ornithine decarboxylase during oncogenic transformation:mechanisms and therapeutic potential[J].Amino Acids, 2007, 33:213-223. [10] Holtta E, Sistonen L, Alitalo K.The mechanisms of ornithine decarboxylase deregulation in c-Ha-ras oncogene-transformed NIH3T3 cells[J].J Biol Chem, 1988, 263:4500-4507. [11]Ignatenko NA, Babbar N, Mehta D, et al.Suppression of polyamine catabolism by activated Ki-ras in human colon cancer cells[J].Molecular Carcinogenesis, 2004, 39:91-102. [12]Funakoshi-tago M, Sumi K, Kasahara AT, et al.Critical roles of Myc-ODC axis in the cellular transformation induced by myeloproliferative neoplasm-associated JAK2 V617F mutant[J].PLoS One, 2013, 8:e52844. [13] Kubota S, Kiyosawa H, Nomura Y, et al.Ornithine decarboxylase overexpression in mouse 10T1/2 fibroblasts:cellular transformation and invasion[J].Journal of The National Cancer Institute, 1997, 89:567-571. [14] Smith MK, Goral MA, Wright JH, et al.Ornithine decarboxylase overexpression leads to increased epithelial tumor invasiveness[J].Cancer Research, 1997, 57:2104-2108. [15]Pegg AE.S-Adenosylmethionine decarboxylase[J].Essays Biochem, 2009, 46:25-45. [16] Williams-ashman HG, Schenone A.Methyl glyoxal bis(guanylhy-drazone)as a potent inhibitor of mammalian and yeast S-adenosy-lmethionine decarboxylases[J].Biochemical and Biophysical Research Communications, 1972, 46:288-295. [17]Pleshkewych A, Kramer DL, Kelly E, et al.Independence of drug action on mitochondria and polyamines in L1210 leukemia cells treated with methylglyoxal-bis(guanylhydrazone)[J].Cancer Research, 1980, 40:4533-4540. [18]Seiler N.Thirty years of polyamine-related approaches to cancer therapy.Retrospect and prospect.Part 2.Structural analogues and derivatives[J].Current Drug Targets, 2003, 4:565-585. [19]Regenass U, Mett H, Stanek J, et al.CGP 48664, a new S-adenosylmethionine decarboxylase inhibitor with broad spectrum antiproliferative and antitumor activity[J].Cancer Research, 1994, 54:3210-3217. [20]Nowotarski SL, Woster PM, Casero RA, JR.Polyamines and cancer:implications for chemotherapy and chemoprevention[J].Expert Reviews in Molecular Medicine, 2013, 15:e3. [21]Pegg AE, Tang KC, Coward JK.Effects of S-adenosyl-1, 8-diamino-3-thiooctane on polyamine metabolism[J].Biochemistry, 1982, 21:5082-5089. [22]Holm I, Persson L, Pegg AE, et al.Effects of S-adenosyl-1, 8-diamino-3-thio-octane and S-methyl-5'-methylthioadenosine on polyamine synthesis in Ehrlich ascites-tumour cells[J].The Biochemical Journal, 1989, 261:205-210. [23]Casero RA, Marton LJ.Targeting polyamine metabolism and function in cancer and other hyperproliferative diseases[J].Nature Reviews Drug Discovery, 2007, 6:373-390. [24] Delcros JG, Tomasi S, Duhieu S, et al.Effect of polyamine homolo-gation on the transport and biological properties of heterocyclic amidines[J].J Med Chem, 2006, 49:232-245. [25] Porter CW, Pegg AE, Ganis B, et al.Combined regulation of ornithine and S-adenosylmethionine decarboxylases by spermine and the spermine analogue N1 N12-bis(ethyl)spermine[J].The Biochemical Journal, 1990, 268:207-212. [26]Jenuwein T, Allis CD.Translating the histone code[J].Science, 2001, 293:1074-1080. [27]Marks P, Rifkind RA, Richon VM, et al.Histone deacetylases and cancer:causes and therapies[J].Nat Rev Cancer, 2001, 3:194-202. [28]Johnstone RW, Licht JD.Histone deacetylase inhibitors in cancer therapy:is transcription the primary target?[J].Cancer Cell, 2003, 4:13-18. [29]Hobbs CA, Paul BA, Gilmour SK.Elevated levels of polyamines alter chromatin in murine skin and tumors without global changes in nucleosome acetylation[J].Experimental Cell Research, 2003, 290:427-436. [30]Hobbs CA, Paul BA, Gilmour SK.Deregulation of polyamine biosynthesis alters intrinsic histone acetyltransferase and deacetylase activities in murine skin and tumors[J].Cancer Research, 2002, 62:67-74. [31]Hobbs CA, Gilmour SK.High levels of intracellular polyamines promote histone acetyltransferase activity resulting in chromatin hyperacetylation[J].J Cell Biochem, 2000, 77:345-360. [32]Shi YJ, Matson C, Lan F, et al.Regulation of LSD1 histone demethylase activity by its associated factors[J].Molecular Cell, 2005, 19:857-864. [33]Huang Y, Gerrne E, Murray Stewart T, et al.Inhibition of lysine-specific demethylase 1 by polyamine analogues results in reexpression of aberrantly silenced genes[J].Proc Natl Acad Sci USA, 2007, 104:8023-8028. [34]Zhu Q, Huang Y, Marton LJ, et al.Polyamine analogs modulate gene expression by inhibiting lysine-specific demethylase 1(LSD1)and altering chromatin structure in human breast cancer cells[J].Amino Acids, 2012, 42:887-898. [35]Pledgie A, Huang Y, Hacker A, et al.Spermine oxidase SMO(PAOh1), Not N1-acetylpolyamine oxidase PAO, is the primary source of cytotoxic H2O2 in polyamine analogue-treated human breast cancer cell lines[J].The Journal of Biological Chemistry, 2005, 280:39843-39851. [36]Tian Y, Wang S, Wang B, et al.Overexpression of SSAT by DENSPM treatment induces cell detachment and apoptosis in glioblastoma[J].Oncology Reports, 2012, 27:1227-1232. [37]Stanic I, Facchini A, Borzi RM, et al.The polyamine analogue N1, N11-diethylnorspermine can induce chondrocyte apoptosis independently of its ability to alter metabolism and levels of natural polyamines[J].J Cell Physiol, 2009, 219:109-116. [38]王世召, 田野, 江荣才, 等.多胺类似物DENSPM对人胶质瘤LN229细胞增殖的抑制作用[J].中华神经外科疾病研究杂志, 2013, 12:101-105. [39]谢松强, 李骞, 张亚宏, 等.萘酰亚胺-多胺缀合物NNINspm通过PI3K/Akt信号通路诱导肝癌细胞凋亡[J].中国药理学通报, 2010, 26:169-174. [40]Yang L, Li W, Tian Z, et al.Mononaphthalimide spermidine conjugate induces cell proliferation inhibition and apoptosis in HeLa cells[J].Toxicology in Vitro, 2011, 25(4):882-889. [41]Yang L, Zhao J, Zhu Y, et al.Reactive oxygen species(ROS)accumulation induced by mononaphthalimide-spermidine leads to intrinsic and AIF-mediated apoptosis in HeLa cells[J].Oncology Reports, 2011, 25:1099-1107. |