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14-3—3σ基因与乙型肝炎病毒相关性肝癌的关系

Progress on the correlation between 14-3-3 sigma gene and hepatitis B virus-related hepatocellular carcinoma
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摘要 HBV感染与人原发性肝细胞癌有病因学联系。14-3-3σ蛋白在细胞周期和细胞凋亡过程中起负调节作用，主要调节G2／M期检查点。在多数肿瘤形成的过程中，14-3-3σ由于高度甲基化而失活，从而促进肿瘤的发生。根据14-3-3σ控制细胞周期、修复DNA损伤、抑制细胞凋亡及促细胞分化和衰老等一些与肿瘤的发病机制有关的生物学特性，有望把14-3-3σ作为抗癌治疗的靶蛋白。此文就近年来有关14-3-3σ基因与HBV相关性肝癌的关系进行了综述。 HBV infection is one of the etiological factors of human hepatoeellular i2areinomai. 14-3-3 sigma protein is a negative regulator of cell cycle and apoptosis, mainly regulating the checkpoint of G2/M. During the formation process of most tumors, 14-3-3 sigma becomes inactive because of hypermethylation, which in turn promotes the development of tumors, Therefore, based on the characteristic of 14-3-3 sigma related with pathogenesis of tumors such as controlling cell cycle, repairing DNA injury, suppressing cell apoptosis as well as promoting differentiation and apolexis, it is hopeful using 14-3-3 sigma as a target protein in anticancer treatment. This article shows the recent researches on 14-3-3 sigma gene and HBV related hepatocellular carcinoma.
作者 苏倩 李旭
机构地区 安徽医科大学第一附属医院感染科
出处 《国际流行病学传染病学杂志》 CAS 2008年第4期259-261,共3页 International Journal of Epidemiology and Infectious Disease
基金 国家自然科学基金（30471518）
关键词 基因 肝细胞癌 肝炎病毒 乙型 甲基化 Gene Hepatocellular carcinoma Hepatitis B virus Methylation
分类号 R735 [医药卫生—肿瘤] R51 [医药卫生—内科学]
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参考文献17

  • 1Herath NI, Leggett BA, MacDonald GA. Review of genetic and epigenetic alterations in hepatocarcinogenesis. J Gastroenterol Hepatol, 2006,21 ( 1 ) : 15-21.
  • 2Ushijima T. Detection and interpretation of altered methylation patterns in cancer cells. Nat Rev Cancer, 2005, 5 (3) : 223-231.
  • 3Sekimoto T, Fukumoto M, Yoneda Y. 14-3-3 suppresses the nuclear localization of threonine 157-phosphorylated p27 (Kipl). EMBO J, 2004, 23(9) : 1934-1942.
  • 4Benzinger A, Muster N, Koch HB, et al. Targeted proteomic analysis of 14-3-3 sigma, a p53 effector commonly silenced in cancer. Mol Cell Proteomics, 2005,4 ( 6 ) : 785-795.
  • 5Kunze E, Schlott T. High frequency of promoter methylation of the 14-3-3 sigma and CAGE-1 genes, but lack of hypermethylation of the caveolin-1 gene, in primary adenocarcinomas and signet ring cell carcinamas of the urinary bladder. Int J Mol Med ,2007,20(4) :557-563.
  • 6Mhawech P, Benz A, Cerato C, et al. Downregulation of 14-3-3 sigma in ovary, prostate and endometrial carcinomas is associated with CpG island methylation. Mod Pathol, 2005,18 (3) : 340-348.
  • 7Henrique R, Jeronimo C, Hoque MO. Frequent 14-3-3 sigma promoter methylation in benign and malignant prostate lesions. DNA Cell Biol, 2005,24(4) :264-269.
  • 8Lodygin D,Yazdi AS,Sander CA,et al. Analysis of 14-3-3 sigma expression in hyperproliferative skin diseases reveals selective loss associated with CpG-methylation in basal cell carcinoma. Oncogene, 2003, 22(35): 5519-5524.
  • 9Bhatia K, Siraj AK, Hussain A, et al. The tumor suppressor gene 14-3-3 sigma is commonly methylated in normal and malignant lymphoid cells. Cancer Epidemiol Biomarkers Prey, 2003, 12 ( 2 ) : 165- 169.
  • 10Moreira JM, Ohlsson G, Rank FE, et al. Down-regulation of the tumor suppressor protein 14-3-3 sigma is a sporadic event in cancer of the breast. Mole Cell Proteomics, 2005,4(4) : 555-569.
国际流行病学传染病学杂志
2008年 第4期

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