3 结束语
总之,肿瘤的形成是一个复杂的过程,ACA对肿瘤形成的抑制存在着多条途径。研究ACA抗肿瘤形成机制,可以准确地瞄准肿瘤发病过程中药物治疗的靶分子,并且为新的基因工程抗癌药物的设计和多种抗癌药物的协和治疗等方面提供新的思路。
【参考文献】
[1] Nakamura Y, Murakami A, Ohto Y,et al. Suppression of tumor promoterinduced oxidative stress and inflammatory responses in mouse skin by a superoxide generation inhibitor 1’acetoxychavicol acetate[J]. Cancer Research,1998,58(21): 48324839.
[2] Takeuchi T, Nakajima M,Morimoto K. Relationship between the intracellular reactive oxygen species and the induction of oxidative DNA damage in human neutrophilslike cells[J]. Carcinogenesis(Lond),1996,17: 15431548.
[3] Lundqvist H, Follin P, Khalfan L,et al. Phorbol myristate acetateinduced NADPH oxidase activity in human neutrophils:only half the story has been told[J]. J.Leukocyte Biol, 1996, 59:270279.
[4] Yamamoto S, Kiyoto I, Aizu E, et al. Differential inhibition by staurosporine, a potent protein kinase C inhibitor of 12Otetradecanoylphorbol13acetatecaused skin tumor promotion, epidermal ornithine decarboxylase induction, hyperplasia and inflammation[J]. Carcinogenesis(Lond).1989, 10: 13151322.
[5] Watababe N, Kataka T, Tajika T, et al. 1’acetoxychavicol acetate as an inhibitor of phagocytosis macrophages[J]. Biosci Biotechnol Biochem, 1995, 59: 15661567.
[6] Wang L D, Lipkin, Mqui S L, et al. labeling index and labeling distribution of cells in esophageal epithelium of individuals a increased risk for esophageal cancer in Huixian China[J]. Cancer Research, 1990,50: 26512653.
[7] Mori H, Sugle N, Yoshimi N, et al. Control of cell proliferation in cancer prevention[J]. Mutat Res, 1999, 428: 291298.
[8] Tanaka T, Kojima T, Morishita Y et al. Inhibitory effects of the natural products indole3carbinol and sinigrin during initiation and promotiom phases of 4nitroquinoline 1oxideinduced rat tongue carcinogenesis[J]. Jap J cancer Res, 1992, 83:835842.
[9] Tanaka T, Kawamori L, Tohnishi M, et al. Chemoprevention of 4nitroquinoline 1oxideinduced oral carcinogenesis by dietary protocatachui acid during initiation and postinitiation phases[J]. Cancer Research, 1994, 54: 23592365.
[10] Klaunig J E. Chemopreventive effects of green tea components on hepatic carcinogenesis[J]. Prev Med, 1992, 21: 510519.
[11]Kawabata K, Tanaka T, Yamamoto T, et al. Suppression of Nnitrosomethylbenzylamineinduced rat esophageal tumorigenesis by dietary feeding of 1’acetoxychavicol acetate[J]. Japanese Journal of Cancer Research, 2000, 91(2): 148155.
[12]Ohnishi M, Tanaka T, Makita H, et al. Chemopreventive effect of a xanthine oxidase inhibitor, 1’acetoxychavicol acetate, on rat oral carcinogenesis[J]. Japanese Journal of cancer research: Gann.1996,87(4):349356.
[13]Tanaka T, Kawabata K, Kakumoto M, et al. Chemoprevention of azoxymethaneinduced rat colon carcinogenesis by a xanthine oxidase inhibitor, 1’acetoxychavicol acetate[J]. Japanese Journal of cancer research: Gann.1997,88(9):821830.
[14]Mori H, Morishita T, Mori Y, et al. Effect of magnesium hydroxide on methylazoxymethanol acetateinduced epithelial proliferation in the large bowels of rats[J]. Cancer Lett, 1992, 62: 4348.
[15]Wang A, Yoshimi N, Tanaka T, et al. Inhibitory effects of magnesium hydroxide on cmyc expression and cell proliferation induced by methylazoxymethanol acetate in rat colon[J]. Cancer Lett, 1993, 75: 7378.
[16]Mori H, Niwa K, Zheng Q, et al. Cell proliferation in cancer prevention: effects of preventive agents on estrogenrelated endometrial carcinogenesis model and on an in vitro model in human colorectal cells[J]. Mutation Research, 2001,480481: 201207.
[17]Ahn D, Putt D, Kresty L, et al. The effects of dietary ellagic acid on rat heparic and esophageal mucosal cytochrome P 450 and phase II enzymes[J]. Carcinogenesis, 1996, 17: 821828.
[18]Wei H, Frenkel K. In vitro formation of oxidized DNA bases in tumor promotertreated mouse skin[J]. Cancer Research, 1991, 51: 44434449,
[19]Shacter E, Weitzman S A, Chronic inflammationand cancer[J]. Oncology, 2002, 16: 217226.
[20]Goto T, Haruma K, Kitadai Y, et al. Enhanced expression of inducible nitric oxide synthase and nitrotyosine in gastric mucosa of gastric cancer patients[J]. Clin, Cancer Res, 1999,5: 14111415.
[21]Maeda H, Akaike T. Nitric oxide and oxygen radicals in infection, inflammation,and cancer[J]. Biochemistry (Mosc.), 1998, 63: 854865.
[22]Ghosh S, May M J, Kopp E B. NFkappa B and Rcl proteins: evolutionarily conserved mediators of immune responses[J]. Annu.Rev.Immunol, 1998, 16: 225260.
[23]Surh Y J, Chun KS, Cha H.H, et al. Molecular mechanism underlying chemopreventive activities of antiinflammatory phytochemicals down regulation of COX2 and iNOS through suppression of NFκB activation Mutat[J]. Res, 2001,480481, 243268.
[24]Pando M P, Verma L M. Signaldependent and independent degradation of free and NFKappa Bbound IkappaBalpha[J]. J Biol Chem, 2000, 275: 2127821286.
[25]Murakami A, Matsumoto K, Koshimizu K, et al. Effects of selected food factors with chemopreventive properties on combined lipopolysaccharide and interferonγinduced IkB degradation in RAW264.7 macrophages[J]. Cancer Letters, (Oxford, United Kingdom) 2003,195(1): 1725.
[26]Moffatt J, Kennedy D O, Kojima A, et al. Involvement of protein tyrosine phosphorylation and reduction of cellular sulfhydryl groups in cell death induced by 1’acetoxychavicol acetate in Ehrlich ascites tumor cells[J]. ChemicoBiological Interactions, 2002,139(2): 215230.