脆性组氨酸三联体基因研究进展

秦阳华; 韩玲

脆性组氨酸三联体基因研究进展

秦阳华 , 韩玲

文章导航 > 国际放射医学核医学杂志 > 2006, 30 > 1: (47-49)

引用本文:

Citation:

脆性组氨酸三联体基因研究进展

秦阳华,
韩玲

200433 上海, 第二军医大学海医系放射医学教研室
中图分类号: Q344⁺.13

Fragile histidine triad gene and tumor

Department of Radiation Medicine, Navy Medicine Faculty, the Second Military Medicial University, Shanghai 200433, China
CLC number: Q344⁺.13

摘要: 恶性转化是复杂的、渐变的过程,涉及许多遗传改变,包括抑癌基因失活、癌基因激活和其他调节基因功能改变。脆性组氨酸三联体(FHIT)基因是一个新发现的抑癌基因,过去近10年的研究表明其和许多肿瘤有密切的关系。本文综述了近几年分子生物学有关FHIT基因研究的最新进展,并侧重描述了其和辐射致癌的关系。
- 基因,脆性组氨酸三联体 /
- 基因,肿瘤抑制 /
- 辐射效应
Abstract: Malignant transformation is a complex multistep process involving numerous genetic changes, which include loss of tumor suppressor gene function, oncogene activation and alteration of modifier genes. During the past decade, evidence has accumulated in support that FHIT, as a new tumor suppressor gene, plays a roll in many tumors. In this review, described the recent findings in the molecular biology of FHIT, with particular focus on its relationship with radiation carcinogenesis.
- Gene,fragile histidine triad /
- Gene,tumor suppressor /
- Radiation effects
本作品遵循Signature-Non-Commercial Use 4.0 International (CC BY-NC 4.0)协议

[1]	Ohta M,Inoue H,Cotticelli MG,et al.The FHIT gene,spanning the chromosome 3p 14.2 fragile site and renal carcinoma-associated t (3;8) breakpoint,is abnormal in digestive tract cancers.Cell,1996,84(4):587-597.
[2]	Sard L,Accornero P,Tornielli S,et al.The tumor-suppressor gene FHIT is involved in the regulation of apoptosis and in cell cycle control.Proc Natl Acad Sci USA,1999,96(15):8489-8492.
[3]	Gopalakrishnan VK,Banerjee AG,Vishwanatha JK,et al.Effect of FHIT gene replacement on growth,cell cycle and apoptosis in pancreatic cancer cells.Pancreatology,2003,3(4):293-302.
[4]	Huang K,Arabshahi A,Wei Y,et al.The mechanism of action of the fragile histidine triad,FHIT:isolation of a covalent adenylyl enzyme and chemical rescue of H96G-FHIT.Biochemistry,2004,43(23):7637-7642.
[5]	Chaudhuri AR,Khan IA,Prasad V,et al.The tumor suppressor protein FHIT.A novel interaction with tubulin.J Biol Chem,1999,274(34):24378-24382.
[6]	Galmarini CM,Kamath K,Vanier-Viornery A,et al.Drug resistance associated with loss of p53 involves extensive alterations in microtubule composition and dynamics.Br J Cancer,2003,88(11):1793-1799.
[7]	Lee YC,Wu CT,Shih JY,et al.Frequent allelic deletion at the FHIT locus associated with p53 overexpression in squamous cell carcinoma subtype of Taiwanese non-small-cell lung cancers.Br J Cancer,2004,90(12):2378-2383.
[8]	Song LY,Yan WS,Deng M,et al.Aberrations in the fragile histidine triad (FHIT) Gene may be involved in lung carcinogenesis in patients with chronic pulmonary tuberculosis.Tumor Biol,2004,25(5-6):270-275.
[9]	Tzao C,Tsai HY,Chen JT,et al.5'CpG island hypermethylation and aberrant transcript splicing both contribute to the inactivation of the FHIT gene in resected non-small cell lung cancer.Eur J Cancer,2004,40(14):2175-2183.
[10]	Lee SH,Kim HY,Kim TJ et al.Aberrant splicing of FHIT transcripts in human gastric cancer cell lines.Res Commun Mol Pathol Pharmacol,2002,112(1-4):39-49.
[11]	Dhillon VS,Shahid M,Husain SA.CpG methylation of the FHIT,FANCF,cyclin-D2,BRCA2 and RUNX3 genes in Granulosa cell tumors (GCTs) of ovarian origin.Mol Cancer,2004,3(1):33.
[12]	Fujishita T,Doi Y,Sonoshita M,et al.Development of spontaneous tumours and intestinal lesions in FHIT gene knockout mice.BrJ Cancer,2004,91(8):1571-1574.
[13]	Kitahashi T,Tsujiuchi T,Satoh K,et al.Aberrant transcription of FHIT gene in intrahepatic cholangiocellular carcinomas induced by N-nitrosobis (2-oxopropyl) amine in hamsters.Exp Toxicol Pathol,2004,56(3):153-157.
[14]	Lubet RA,Huebner K,Fong LY,et al.4-Hydroxybutyl (butyl) nitrosamine-induced urinary bladder cancers in mice:characterization of FHIT and survivin expression and chemopreventive effects of indomethacin.Carcinogenesis,2005,26(3):571-578.
[15]	Zanesi N,Fidanza.V,Fong LY,et al.The tumor spectrum in FHITdeficient mice.Proc Natl Acad Sci USA,2001,98(18):10250-10255.
[16]	Dano L,Guilly MN,Muleris M,et al.CGH analysis of radon-induced rat lung tumors indicates similarities with human lung cancers.Genes Chromosomes Cancer,2000,29(1):1-8.
[17]	林亚华,潘真,韩玲,等.⁶⁰Coγ射线照射诱发小鼠恶性肿瘤.第二军医大学学报,2003,24(7):738-741.
[18]	熊杰,韩玲,高伟,等.⁶⁰Coγ射线照射对人脆性组胺酸基因表达的影响.第二军医大学学报,2005,26(5):471-475.
[19]	Dumon KR,Ishii H,Fong LY,et al.FHIT gene therapy prevents tumor development in FHIT-deficient mice.Proc Natl Acad Sci USA,2001,98(18):3346-3351.
[20]	Ishii H,Zanesi N,Vecchione A,et al.Regression of upper gastric cancerin mice by FHIT gene delivery.FASEB J,2003,17(12):1768-1770.

[1]	林向飞 , 骆丹 . MDM2基因与肿瘤放射生物效应. 国际放射医学核医学杂志, 2007, 31(2): 118-121.
[2]	苑宾 , 王宝勤 , 李雨民 , 鞠桂芝 . 辐射诱导细胞凋亡的基因调控. 国际放射医学核医学杂志, 1998, 22(6): 269-273.
[3]	杨剑 , 韩玲 . 脆性组氨酸三联体与细胞信号转导研究进展. 国际放射医学核医学杂志, 2007, 31(3): 173-175.
[4]	王铭蔚 , 王蕊 , 衣峻萱 , 金顺子 . Hippo信号通路的调控机制及其在肿瘤细胞辐射效应中作用的研究进展. 国际放射医学核医学杂志, 2022, 46(12): 765-772. doi: 10.3760/cma.j.cn121381-202204004-00250
[5]	游洋 , 郭海卓 , 金顺子 . 微小RNA在电离辐射和肿瘤中的作用. 国际放射医学核医学杂志, 2009, 33(4): 243-245. doi: 10.3760/cma.j.issn.1673-4114.2009.04.016
[6]	王利利 , 涂彧 , 周菊英 , 俞志英 , 秦颂兵 , 徐晓婷 , 李莉 . 硫酸镁对大鼠急性放射性脑损伤后脂质过氧化的抑制作用. 国际放射医学核医学杂志, 2007, 31(1): 37-39,54.
[7]	周继文 , 卢正福 . 胎内照射的辐射效应. 国际放射医学核医学杂志, 1995, 19(1): 25-28.
[8]	肖瑶 , 韩玲 . 电离辐射诱导旁效应的研究现状. 国际放射医学核医学杂志, 2007, 31(5): 303-306.
[9]	张晓英 , 廖端芳 . 氡及其子体辐射诱发的非癌变效应. 国际放射医学核医学杂志, 2009, 33(1): 47-49. doi: 10.3760/cma.j.issn.1673-4114.2009.01.047
[10]	李继涛 , 何明远 , 袁德晓 , 沈波 , 邵春林 . p53调控的能量代谢对辐射效应的影响. 国际放射医学核医学杂志, 2012, 36(6): 380-384. doi: 10.3760/cma.j.issn.1673-4114.2012.06.014

点击查看大图

计量

文章访问数: 1006
HTML全文浏览量: 87
PDF下载量: 2

脆性组氨酸三联体基因研究进展

秦阳华
韩玲

200433 上海, 第二军医大学海医系放射医学教研室

收稿日期: 2005-06-05

关键词:

摘要: 恶性转化是复杂的、渐变的过程,涉及许多遗传改变,包括抑癌基因失活、癌基因激活和其他调节基因功能改变。脆性组氨酸三联体(FHIT)基因是一个新发现的抑癌基因,过去近10年的研究表明其和许多肿瘤有密切的关系。本文综述了近几年分子生物学有关FHIT基因研究的最新进展,并侧重描述了其和辐射致癌的关系。