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1.原文来自PLoS One，由干细胞之家成员jiandong2001翻译。/ l7 p2 n2 w/ M* \, v3 D
2.标题：Epithelial to Mesenchymal Transition Is Mechanistically Linked with Stem Cell Signatures in Prostate Cancer Cells; y- K& V, C# t. l' S% F( D' R
3.译文：9 O, `- v& P3 I2 |8 F, J
背景： 前列腺癌目前的治疗方法还是比较有效的，但是，复发的肿瘤对去势治疗耐受以及随之而来的转移导致患者预后不良，因此，迫切需要明确肿瘤复发的机制，用于开发新的治疗方法。前列腺癌复发转移与前列腺癌干细胞或肿瘤起始细胞密切相关，这部分细胞可能具有表皮间充质转变（EMT）的表型特征。越来越多的证据提示具有EMT表型的细胞具有许多肿瘤干细胞样细胞的生物学特征。
+ q% j4 J2 W/ v: t/ F方法/发现： 本研究中，作者发现：具有EMT表型的前列腺癌细胞表现出干细胞样细胞的特征，包括Sox2, Nanog, Oct4, Lin28B 和/或 Notch1表达增加，同时集落及肿瘤球形成能力、小鼠体内的成瘤性均增强，这部分细胞表达 miR-200 和/或 let-7家族的能力下降。通过使 miR-200 重新表达可逆转EMT，从而可抑制EMT型细胞的瘤球形成能力，降低Notch1 及 Lin28B的表达。Lin28B表达的下调可使let-7表达增强，这与自我更新能力被抑制有关。
* q* Q" l- y. q. m结论/意义：这些结果提示miR-200在联系前列腺癌肿瘤干细胞样细胞与EMT样细胞特征标签中扮演着重要的角色。通过使用新的治疗方法逆转EMT，选择性消除肿瘤干细胞样细胞，特别是清除这些被仍为是肿瘤进展与复发根源的细胞，将有利于防止肿瘤复发。
, t" @) s6 }. s d0 ^( m4.原文：
+ i6 T. A# j0 k1 Y! F8 ~Background: Current management of patients diagnosed with prostate cancer (PCa) is very effective; however, tumor recurrence with Castrate Resistant Prostate Cancer (CRPC) and subsequent metastasis lead to poor survival outcome, suggesting that there is a dire need for novel mechanistic understanding of tumor recurrence, which would be critical for designing novel therapies. The recurrence and the metastasis of PCa are tightly linked with the biology of prostate cancer stem cells or cancer-initiating cells that is reminiscent of the acquisition of Epithelial to Mesenchymal Transition (EMT) phenotype. Increasing evidence suggests that EMT-type cells share many biological characteristics with cancer stem-like cells.0 V G* ]5 E' y, ~5 d
Methodology/Principal Findings: In this study, we found that PCa cells with EMT phenotype displayed stem-like cell features characterized by increased expression of Sox2, Nanog, Oct4, Lin28B and/or Notch1, consistent with enhanced clonogenic and sphere (prostasphere)-forming ability and tumorigenecity in mice, which was associated with decreased expression of miR-200 and/or let-7 family. Reversal of EMT by re-expression of miR-200 inhibited prostasphere-forming ability of EMT-type cells and reduced the expression of Notch1 and Lin28B. Down-regulation of Lin28B increased let-7 expression, which was consistent with repressed self-renewal capability.
* t1 i, y& D0 OConclusions/Significance: These results suggest that miR-200 played a pivotal role in linking the characteristics of cancer stem-like cells with EMT-like cell signatures in PCa. Selective elimination of cancer stem-like cells by reversing the EMT phenotype to Mesenchymal-Epithelial Transition (MET) phenotype using novel agents would be useful for the prevention of tumor recurrence especially by eliminating those cells that are the ‘‘Root Cause’’ of tumor development and recurrence.
7 F( Y' D0 d, s* P9 ]( K& g5.本文题目中的Signatures，大家觉得怎么翻译比较合适呢？
1 f7 l i2 Y0 l5 Y6.原文附上！ |
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发表于 2011-1-1 10:53
