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三叶草王铁虫 (正式写手)
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[求助]
英文翻译中文
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The incidence rate of lung cancer has increased over the past decades in China in association with high mortality rates.Non-small-cell lung cancer (NSCLC) is the major histological class accounting for 80% of all lung cancers. Despite advances in multimodality therapies, surgery remains the primary treatment for NSCLC patients with generally unsatisfactory results in advanced disease. New effective therapeutic strategies are urgently needed,and further research on the molecular mechanisms underlying lung cancer is essential. Alterations in growth regulatory signaling pathways play an important role in the pathogenesis of NSCLC. Numerous reports have shown an association between aberrant activation of the Wingless-type (Wnt) signaling pathway and carcinogenesis including that of NSCLC . The Wnt family is a group of secreted signaling molecules that mediate a variety of cellular processes through canonical and/or noncanonical pathways .In the canonical pathway, the Wnt ligand binds directly to the cysteinerich extracellular domain of Frizzled (Fz), resulting in b-catenin stabilization and accumulation in the cytoplasm. The cytoplasmic b-catenin translocates into the nucleus and binds to Tcf/Lef transcription factors, forming a heterodimeric complex that further activates the transcription of important downstream target genes. Aberrant Wnt/b-catenin signaling has been shown to promote cancer cell growth and is associated with poor prognosis in NSCLC . Noncanonical pathways are referred to asb-catenin-independent Wnt signaling. The down-regulation of Wnt antagonists is a common mechanism of aberrant activation of the Wnt signaling pathway. As a major antagonist, Wnt inhibitory factor-1 (WIF-1) is silenced by promoter methylation in NSCLC. However, the mechanism underlying the over-methylation of the WIF-1 gene remains unclear. DNA methylation involves the transfer of a methyl group from the methyl donor S-adenosyl methionine to the 5 position on the cytosine ring, and is accomplished by DNA methyltransferases (DNMTs). Three catalytically active DNMTs, DNMT1, DNMT3A and DNMT3B, have been identified in mammals[8]. The mRNA levels of DNMT1, DNMT3A, and DNMT3B are reportedly elevated in various malignanciesand have been correlated with hypermethylation of tumor suppressor genes. |
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至尊木虫 (知名作家)
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- 翻译EPI: 1690
- 应助: 452 (硕士)
- 金币: 31580.9
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- 注册: 2014-07-17
- 专业: 肿瘤发生
【答案】应助回帖
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真强必胜: 金币+5, 谢谢 2014-08-21 08:15:56
三叶草王: 金币+20, 翻译EPI+1, ★★★★★最佳答案 2014-08-22 18:31:10
真强必胜: 金币+5, 谢谢 2014-08-21 08:15:56
三叶草王: 金币+20, 翻译EPI+1, ★★★★★最佳答案 2014-08-22 18:31:10
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在过去几十年，中国的肺癌发病率已有明显上升，并伴有高死亡率。NSCLC是肺癌的组织学类型，约占所以肺癌的80％。虽然在联合治疗方面取得了进展，但手术仍然是肺癌治疗的主要手段，但手术对晚期肺癌疗效总体来说是不满意的。急需新型而有效的治疗措施，而对引发肺癌的分子机制的进一步研究又是必需的。 生长调节信号通路的变化在NSCLC发病机制中发挥重要作用。许多报告表明，Wnt信号通路的异常激活与包括NSCLC在内的癌症发病之间有关联。Wnt家族由一组分泌型信号分子组成，可以通过经典及非经典途径而介导许多细胞过程。在经典途径，Wnt配体直接与Frizzled（Fz）的富含半胱氨酸的胞外域结合，导致β－catenin的稳定性增加并于细胞质中积聚。β－catenin由细胞质转位入细胞核，并与TCF/LEF转录因子结合，形成一异聚体复合物，后者进一步激活重要下游基因的转录。已经发现Wnt/β－catenin异常可以促进癌症细胞的生长并与NSCLC预后差相关。非经典途径则是指非β－catenin依赖性Wnt信号途径。 对Wnt拮抗剂的下调是引起Wnt信号通路异常激活的一种常见机制。Wnt抑制因子－1（WIF-1）是一种主要的拮抗剂，在NSCLC中通过对其启动子的甲基化而被静默。然而，引起WIF-1基因过度甲基化的机制目前尚不清楚。DNA甲基化包括一甲基基团由甲基供体S-腺苷甲硫氨酸转移至胞嘧啶环之第5位置，此反应由DNA甲基转移酶（DNMTs）完成。在哺乳类已经发现有三种具有催化活性的DNMTs，分别为DNMT1, DNMT3A和DNMT3B。有报告表明，在各种恶性肿瘤中DNMT1, DNMT3A和DNMT3B mRNA水平提高，而且与肿瘤抑制基因的超甲基化相关。 |
2楼2014-08-20 23:28:22
