Suppression of cell growth and invasion by miR-205 in breast cancer.
Suppression of cell growth and invasion by miR-205 in breast cancer.
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作者：
microRNA（miRNAs）是一类能够在转录后水平沉默基因表达的内源性小分子非编码RNA。在这项研究中，我们报告了miR-205在乳腺肿瘤中的表达显著低于匹配的正常乳腺组织。类似地，包括MCF-7和MDA-MB-231的乳腺癌细胞系比非恶性MCF-10A细胞表达更低水平的miR-205。有趣的是，miR-205的异位表达显著抑制细胞增殖和锚定非依赖性生长以及细胞侵袭。此外，动物模型表明miR-205抑制肺转移。最后，蛋白质印迹结合荧光素酶报告基因分析证明ErbB 3和血管内皮生长因子A（VEGF-A）是miR-205的直接靶点，并且这种miR-205介导的抑制可能是通过与ErbB 3和VEGF-A的3 '-非翻译区（3-UTR）中推定的miR-205结合位点的直接相互作用。总之，这些结果表明miR-205是乳腺癌中的肿瘤抑制因子。
MicroRNAs (miRNAs) are endogenously small non-coding RNAs which are capable of silencing gene expression at the posttranscriptional level. In this study, we report that miR-205 is significantly underexpressed in breast tumor compared to the matched normal breast tissue. Similarly, breast cancer cell lines including MCF-7 and MDA-MB-231 express a lower level miR-205 than the non-malignant MCF-10A cells. Of interest, ectopic expression of miR-205 significantly inhibits cell proliferation and anchorage independent growth as well as cell invasion. Furthermore, the animal model indicates that miR-205 suppresses lung metastasis. Finally, western blot combined with the luciferase reporter assays demonstrate that ErbB3 and vascular endothelial growth factor A (VEGF-A) are direct targets for miR-205 and this miR-205-mediated suppression is likely through the direct interaction with the putative miR-205 binding site in the 3’-untranslated region (3-UTR) of ErbB3 and VEGF-A. Together, these results suggest that miR-205 is a tumor suppressor in breast cancer.
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影响因子：
14.9
作者：
Chen C;Ridzon DA;Broomer AJ;Zhou Z;Lee DH;Nguyen JT;Barbisin M;Xu NL;Mahuvakar VR;Andersen MR;Lao KQ;Livak KJ;Guegler KJ
通讯作者：
Guegler KJ
影响因子：
4.5
作者：
Cai, XZ;Hagedorn, CH;Cullen, BR
通讯作者：
Cullen, BR
DOI：
10.1073/pnas.91.17.8132
发表时间：
1994-08-16
影响因子：
11.1
作者：
GUY, PM;PLATKO, JV;CARRAWAY, KL
通讯作者：
CARRAWAY, KL
影响因子：
4.5
作者：
Bracht, J;Hunter, S;Pasquinelli, AE
通讯作者：
Pasquinelli, AE
影响因子：
14.9
作者：
Griffiths-Jones S;Grocock RJ;van Dongen S;Bateman A;Enright AJ
通讯作者：
Enright AJ