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三葉草王

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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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三葉草王: 金幣+20, 翻譯EPI+1, ★★★★★最佳答案 2014-08-22 18:31:10

在過去幾十年，中國的肺癌發(fā)病率已有明顯上升，并伴有高死亡率。NSCLC是肺癌的組織學(xué)類型，約占所以肺癌的80％。雖然在聯(lián)合治療方面取得了進(jìn)展，但手術(shù)仍然是肺癌治療的主要手段，但手術(shù)對(duì)晚期肺癌療效總體來說是不滿意的。急需新型而有效的治療措施，而對(duì)引發(fā)肺癌的分子機(jī)制的進(jìn)一步研究又是必需的。

生長調(diào)節(jié)信號(hào)通路的變化在NSCLC發(fā)病機(jī)制中發(fā)揮重要作用。許多報(bào)告表明，Wnt信號(hào)通路的異常激活與包括NSCLC在內(nèi)的癌癥發(fā)病之間有關(guān)聯(lián)。Wnt家族由一組分泌型信號(hào)分子組成，可以通過經(jīng)典及非經(jīng)典途徑而介導(dǎo)許多細(xì)胞過程。在經(jīng)典途徑，Wnt配體直接與Frizzled（Fz）的富含半胱氨酸的胞外域結(jié)合，導(dǎo)致β－catenin的穩(wěn)定性增加并于細(xì)胞質(zhì)中積聚。β－catenin由細(xì)胞質(zhì)轉(zhuǎn)位入細(xì)胞核，并與TCF/LEF轉(zhuǎn)錄因子結(jié)合，形成一異聚體復(fù)合物，后者進(jìn)一步激活重要下游基因的轉(zhuǎn)錄。已經(jīng)發(fā)現(xiàn)Wnt/β－catenin異�？梢源龠M(jìn)癌癥細(xì)胞的生長并與NSCLC預(yù)后差相關(guān)。非經(jīng)典途徑則是指非β－catenin依賴性Wnt信號(hào)途徑。

對(duì)Wnt拮抗劑的下調(diào)是引起Wnt信號(hào)通路異常激活的一種常見機(jī)制。Wnt抑制因子－1（WIF-1）是一種主要的拮抗劑，在NSCLC中通過對(duì)其啟動(dòng)子的甲基化而被靜默。然而，引起WIF-1基因過度甲基化的機(jī)制目前尚不清楚。DNA甲基化包括一甲基基團(tuán)由甲基供體S-腺苷甲硫氨酸轉(zhuǎn)移至胞嘧啶環(huán)之第5位置，此反應(yīng)由DNA甲基轉(zhuǎn)移酶（DNMTs）完成。在哺乳類已經(jīng)發(fā)現(xiàn)有三種具有催化活性的DNMTs，分別為DNMT1, DNMT3A和DNMT3B。有報(bào)告表明，在各種惡性腫瘤中DNMT1, DNMT3A和DNMT3B mRNA水平提高，而且與腫瘤抑制基因的超甲基化相關(guān)。

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2樓2014-08-20 23:28:22