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三葉草王

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Concurrent aberrant activation of the Wnt pathway and downregulation of Wnt antagonists are common in cancer cells.
Silencing or downregulation of the WIF-1 gene by promoter hypermethylation has been detected in several malignancies including
lung cancer, and it has been associated with tumorigenesis. In the present study, three DNMTs (DNMT1, DNMT3A and DNMT3B) were found to be up-regulated in NSCLC tumor tissues and their suppression restored the expression of WIF-1 in NSCLC cells. Because DNMT3A and DNMT3B are negatively regulated by miR-29s, we explored the involvement of the miR-29 family in the aberrant regulation of Wnt signaling. Mir-29 family members have been described as tumor suppressor genes and their expression is down-regulated in several cancers, including NSCLC,cholangiocarcinoma[27]and acute myeloid leukemia[28]. We observed that the expression of miR-29s was positively correlated with the expression of WIF-1 in NSCLC tissue. The results of MSP and Western blotting indicated that miR-29s contribute to the
reduction of promoter methylation of the WIF-1 gene and positively regulate the expression of WIF-1. These results confirmed
our hypothesis and link miR-29s to the Wnt pathway. In the present study, we showed that miR-29s inhibited Wnt/bcatenin signaling as shown by the effect of overexpression of miR-29 family members on the downregulation ofb-catenin expression. In agreement with previous studies [14,29,30], we also showed that miR-29s inhibit cell proliferation and induce apoptosis in NSCLC cells. A previous study showed that miR-29s sensitize tumor cell to apoptosis by targeting Mcl-1 or the p53 pathway.Our results showed that WIF-1 knockdown abolishes these effects of miR-29s, suggesting that inhibition of Wnt signaling could be another potential mechanism mediating the anti-tumor effects of miR-29s.

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1樓 2014-08-25 18:52:22

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【答案】應(yīng)助回帖

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RXMCDM: 金幣+1, 多謝應(yīng)助！ 2014-08-27 10:22:25
三葉草王: 金幣+20, 翻譯EPI+1, ★★★★★最佳答案 2014-08-27 15:52:11

在癌癥細(xì)胞中，同時出現(xiàn)Wnt信號通路的異常激活和Wnt拮抗劑的下調(diào)是（很）常見的。
在包括肺癌在內(nèi)的幾種惡性腫瘤中，發(fā)現(xiàn)可以通過啟動子超甲基化而使WIF-1基因靜默或下調(diào)，而且與腫瘤發(fā)生具有相關(guān)性。在本研究中，(我們)發(fā)現(xiàn)在NSCLC腫瘤組織中三種DNMTs（DNMT1、DNMT3A和DNMT3B）有向上調(diào)節(jié)，而且抑制它們表達(dá)后可以恢復(fù)WIF-1在NSCLC細(xì)胞中的表達(dá)。因為DNMT3A和DNMT3B受miR-29s的負(fù)調(diào)節(jié)，我們探討了miR-29家族在Wnt信號通路異常調(diào)節(jié)中的參與情況。miR29家族成員被認(rèn)為是腫瘤抑制基因，其表達(dá)在數(shù)種癌癥中是向下調(diào)節(jié)的，包括NSCLC、膽管癌[27]和急性粒細(xì)胞性白血病[28]。我們觀察到，miR-29s在NSCLC組織中與WIF-1的表達(dá)呈正相關(guān)。MSP結(jié)果和Western印跡表明，miR-29s可以引起WIF-1基因啟動子甲基化降低并正向調(diào)節(jié)WIF-1的表達(dá)。這些結(jié)果證實了我們的假說并將miR-29s與Wnt信號通路聯(lián)系起來。在本研究中，我們表明，miR-29s可以抑制Wnt/β-catenin信號通路，體現(xiàn)在miR-29家族成員過度表達(dá)對β-catenin表達(dá)的向下調(diào)節(jié)作用。與以前的研究一致 [14,29,30]，我們也發(fā)現(xiàn)miR-29s在NSCLC細(xì)胞中可以抑制細(xì)胞增殖并誘導(dǎo)其凋亡。曾有一研究表明，miR-29s可以通過靶向Mcl-1或p53通路而使腫瘤細(xì)胞更易于發(fā)生凋亡。我們的結(jié)果表明敲減WIF-1可以消除miR-29s的這些作用，提示抑制Wnt信號通路可能是介導(dǎo)miR-29s抗腫瘤作用的另一可能（潛在）機制。

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2樓2014-08-27 09:02:15