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活性氧与肿瘤研究进展

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基因组学论文

学 院 生命科学学院

专 业 生物科学

年 级 生科2班

姓 名 方海燕

论文题目 活性氧与肿瘤研究进展

指导教师 陈磊 职称 讲师

学号: 20145071235 实用

文档 2017 年 5 月 3 日

目 录

【摘要】 ................................................................. 3

Abstract ................................................................. 3

Keywords: ................................................................ 4

1概述 .................................................................... 4

2肿瘤患者氧化还原状态改变 ................................................ 4

3肿瘤患者ROS增多机制 .................................................... 5

3.1遗传分子生物学改变 ................................................ 5

3.2能量代谢改变 ...................................................... 5

3.3炎性因子参与 ...................................................... 5

3.4杭肿瘤药物使用 .................................................... 5

4 ROS与肿瘤生物学特性关系 ............................................... 5

4. 1与肿瘤形成研究发现 ............................................... 5

4.1.1脂质过氧化生物膜磷脂中的多不饱和脂肪酸 ...................... 5

4.1.2 DNA损伤ROS通过诱导核DNA ( nDNA ) .......................... 5

4.1.3蛋白质破坏 .................................................. 5

4.2 ROS与肿瘤转移 .................................................... 6

5 ROS与肿瘤治疗 .......................................................... 6

6结语 .................................................................... 6

参考文献 ................................................................. 7

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活性氧与肿瘤研究进展

姓名:方海燕 学号:20145071235

学院:生命科学学院

指导老师:陈磊 职称:讲师

【摘要】目的:探讨活性氧与肿瘤的发生、发展和治疗之间的关系。方法:应用 PubMed和 CNKI期刊全文数据库检索系统,以“活性氧和肿瘤”为关键词,检索2000-01-2013-06的相关文献。共检索到英文文献29条,中文文献330条,纳入标准:1)活性氧与肿瘤发生;2)活性氧与肿瘤转移;3)活性氧与肿瘤治疗。根据纳入的标准,最后分析文献27篇。结果:肿瘤患者体内氧化还原失衡,表现为氧化应激水平增高,国内外在胃肠道肿瘤、舌癌和乳腺癌等的研究中均发现了氧化应激状态改变。肿瘤患者 活 性 氧 增

多 的 机 制 主 要 集 中 在 如 下 几 个 方 面:1)遗 传 分 子 生 物 学

的 改 变,包 括 转 入 因 子Nrf2及其抑制蛋白 Keap1、RAS途径的相关突变,癌基因蛋白(比如 Raf、Mos、MEK 和 Myc)的过度表达,抑癌基因(如p53)的沉默;2)肿瘤细胞处于高代谢状态,患者正常营养素摄取减少,引起活性氧的堆积;3)免疫系统非特异性的慢性激活,产生过多的前炎性因子;4)抗肿瘤药物特别是多柔比星和顺铂等的使用。活性氧与肿瘤生物学特性密切相关。一方面,它通过脂质过氧化、DNA 损伤和蛋白质破坏等参与肿瘤的形成;另一方面,活性氧也参与肿瘤的转移,这不仅表现在其清除剂可以降低细胞转移能力,也包括其可以调节肿瘤细胞迁移和侵袭;再者,活性氧和转录因子 Snial相互作用可以诱导上皮细胞间充质转化的产生。活性氧的作用与其浓度有关,高浓度的活性氧可能导致细胞凋亡,而低浓度可致细胞增殖和癌变,国内外研究发现许多抗肿瘤药物通过增加细胞内活性氧的产生来诱导肿瘤细胞凋亡,如乙烷硒啉、三氧化二砷、顺铂、柔红霉素和5-FU 等。

结论:活性氧不仅影响肿瘤的生物学特性,而且与肿瘤的治疗有密切关系,寻找合适的活性氧浓度,将为肿瘤的防治提供帮助。

【关键词】 肿瘤;活性氧;治疗;综述文献。

Abstract:OBJECTIVE; To discuss the relationship between reactive oxygen

species (ROS) and tumor, including the development,metastasis and

treatment of tumor. METHODS; Using "reactive oxygen species and tumor"

as key words to trace related papers from January 2000 to June 2013 in

the database system of PubMed and CNKI. Thirty-nine literatures were

finally selected according to the inclusion criteria as follows; 1)

reactive oxygen species and development of tumor;2) reactive oxygen

species and metastasis of tumor; 3)reactive oxygen species and treatment

of tumor. RESULTS; Tumor patients suffered from redox imbalance,

manifesting as increasing of the oxidative stress level. Domestic and

foreign studies of gastrointestinal tumor tonguc carcinoma brcast cancer

all found the change of oxidative stress level. The main mechanisms why 实用

文档 reactive oxygen species (ROS) arc ample in tumor patients arc as follows:1)

the change of genetic molecularbiology, including relative mutations of

transcription factor Nrf2,its inhibitor protein Kcapl and in RAS pathway,

overexpression of oncogene protein(such as Raf, Mos, MEK and Myc) and

silence of tumor suppressor gene(such as p53);2) tumor cells arc in high

metabolic state, thus patients obtain inadequate nutrition and result to

the accumulation of ROS;3) chronic and nonspecific activation of immune

system gives birth to abundant prion flam matory cytokines;1)the use of

antitumor drugs, especially doxorubicin and cisplatin. ROS arc closely

related to tumor biological characteristics. On the one hand ROS involved

in the development of tumor by mechanisms of lipid peroxidation, DNA

damage and protein injury. On the other hand they also participated in

the metastasis of tumor. For instance,its scavenger could decrease the

metastasis of tumor. Besides, ROS can regulate migration and invasion of

tumor. What’s more, the interaction of ROS and transcription factor Snail

can induce the production of epithelial mesenchymal transition (EM丁).It

is noticeable that the action of ROS is related to their concentration,

In other words, high concentration may lead to cell apoptosis, while low

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