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liruihan铁杆木虫 (正式写手)
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【转帖】Cancer Research：microRNA-155促进肿瘤发生 或为联系炎症和癌症桥梁 已有3人参与
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近日，国际学术期刊《癌症研究》（Cancer Research）发表了中科院上海生命科学研究院生化与细胞所刘默芳实验室和王恩多研究组合作的最新研究成果，该工作揭示了microRNA-155在乳腺癌细胞中的功能和作用机制。 microRNA-155是一种多功能的microRNA，它调控造血细胞和免疫细胞的发育分化，在炎症、抗体合成等多种免疫反应中发挥重要作用；同时，microR-155在淋巴癌、乳腺癌、肺癌、结肠癌等多种癌组织或细胞系中高表达，但目前对它在癌症尤其是乳腺癌中的功能机制还很不清楚。 该所刘默芳和王恩多联合培养的博士研究生蒋帅等通过分子生物学、细胞生物学及肿瘤生物学等一系列方法技术，发现microRNA-155促进乳腺癌细胞的增殖、soft-agar集落生长，并在人乳腺癌裸鼠移植模型中刺激肿瘤生长，表现为癌基因（oncogene）作用；分析microRNA-155在乳腺癌细胞中的分子机制，并结合乳腺癌组织样本分析结果表明，负调控肿瘤抑制基因socs1是其发挥致癌作用的分子机制。 此外，该研究还证明了microRNA-155通过扩大炎症效应促进肿瘤发生，可能是炎症和癌症之间的一个桥梁。虽然文献上已有很多证据表明免疫-炎症-肿瘤之间的内在联系，但对炎症诱发肿瘤发生的分子机制的了解目前仍有许多空白。该工作发现了microRNA调控介入炎症和癌症之间，对了解炎症相关肿瘤的发生机制具有重要意义。 |
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qqsvery
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小木虫(金币+0.5):给个红包，谢谢回帖交流
amisking(金币+4): 2010-04-13 11:26
小木虫(金币+0.5):给个红包，谢谢回帖交流
amisking(金币+4): 2010-04-13 11:26
这项研究有利于我们理解炎症是否诱发导致癌症。 MicroRNA-155 附上原文出处： Cancer Research, doi ：10.1158/0008-5472.CAN-09-4250 MicroRNA-155 Functions as an OncomiR in Breast Cancer by Targeting the Suppressor of Cytokine Signaling 1 Gene Shuai Jiang1,2,3, Hong-Wei Zhang4, Ming-Hua Lu1,2, Xiao-Hong He2,5, Yong Li6, Hua Gu3,7, Mo-Fang Liu1,2,3 and En-Duo Wang1 Authors' Affiliations: 1 State Key Laboratory of Molecular Biology, 2 Core Facility for Noncoding RNA, and 3 Center of Cell Signaling, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences; 4 Department of General Surgery, Zhongshan Hospital Affiliated to Fudan University, Shanghai, China; 5 College of Life Sciences, Lanzhou University, Lanzhou, China; 6 Department of Biochemistry and Molecular Biology and Center for Genetics and Molecular Medicine, School of Medicine, University of Louisville, Louisville, Kentucky; and 7 Department of Microbiology, Columbia University College of Physicians and Surgeons, New York, New York Corresponding Author: Mo-Fang Liu, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai 200031, China. Phone: 86-21-54921146; Fax: 86-21-54921011; E-mail: mfliu@sibs.ac.cn. MicroRNA-155 (miR-155) is overexpressed in many human cancers; however, the mechanisms by which miR-155 functions as a putative oncomiR are largely unknown. Here, we report that the tumor suppressor gene suppressor of cytokine signaling 1 (socs1) is an evolutionarily conserved target of miR-155 in breast cancer cells. We found that mir-155 expression is inversely correlated with socs1 expression in breast cancer cell lines as well as in a subset of primary breast tumors. We also identified a 24AG mutation in the miR-155 binding site of the SOCS1 3' untranslated region in a breast tumor that reduced miR-155 repression, implicating a mechanism for miRNA targets to avoid repression. Ectopic expression of miR-155 significantly promoted the proliferation of breast cancer cells, the formation of soft agar foci in vitro, and the development of tumors in nude mice. In breast cancer cells, RNA interference silencing of socs1 recapitulates the oncogenic effects of miR-155, whereas restoration of socs1 expression attenuates the protumorigenesis function of miR-155, suggesting that miR-155 exerts its oncogenic role by negatively regulating socs1. Overexpression of miR-155 in breast cancer cells leads to constitutive activation of signal transducer and activator of transcription 3 (STAT3) through the Janus-activated kinase (JAK) pathway, and stimulation of breast cancer cells by the inflammatory cytokines IFN- and interleukin-6 (IL-6), lipopolysaccharide (LPS), and polyriboinosinic:polyribocytidylic acid [poly(I:C)] significantly upregulates mir-155 expression, suggesting that miR-155 may serve as a bridge between inflammation and cancer. Taken together, our study reveals that miR-155 is an oncomiR in breast cancer and that miR-155 may be a potential target in breast cancer therapy. [ Last edited by qqsvery on 2010-4-14 at 14:16 ] |
2楼2010-04-05 21:47:32
刚好研究炎症与肿瘤 3楼2010-04-08 12:49:54
4楼2010-04-12 22:48:47
qqsvery
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5楼2010-04-14 14:15:50
6楼2010-04-14 16:07:20
