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本文引用的文献

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The expanding role of miR-302-367 in pluripotency and reprogramming.miR-302-367 在多能性和重编程中的扩展作用。
Cell Cycle. 2012 Apr 15;11(8):1517-23. doi: 10.4161/cc.19846.
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miR-125b targets ARID3B in breast cancer cells.微小RNA-125b在乳腺癌细胞中靶向作用于AT丰富结合域蛋白3B。
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A novel role of miR-302/367 in reprogramming.miR-302/367 在重编程中的新作用
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MiR-21 is involved in cervical squamous cell tumorigenesis and regulates CCL20.微小RNA-21参与宫颈鳞状细胞肿瘤发生并调节趋化因子配体20。
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MiR-125b promotes proliferation and migration of type II endometrial carcinoma cells through targeting TP53INP1 tumor suppressor in vitro and in vivo.miR-125b 通过靶向 TP53INP1 肿瘤抑制因子在体内外促进 II 型子宫内膜癌细胞的增殖和迁移。
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The miR 302-367 cluster drastically affects self-renewal and infiltration properties of glioma-initiating cells through CXCR4 repression and consequent disruption of the SHH-GLI-NANOG network.miR 302-367 簇通过抑制 CXCR4 及其随后破坏 SHH-GLI-NANOG 网络,极大地影响了神经胶质瘤起始细胞的自我更新和浸润特性。
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Multiple targets of miR-302 and miR-372 promote reprogramming of human fibroblasts to induced pluripotent stem cells.miR-302 和 miR-372 的多个靶标促进人成纤维细胞重编程为诱导多能干细胞。
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miRNA-302-367 簇通过 novel target AKT1 抑制宫颈癌细胞的增殖。

The microRNA-302-367 cluster suppresses the proliferation of cervical carcinoma cells through the novel target AKT1.

机构信息

Department of Reproductive Medicine, First Affiliated Hospital, Xi'an Jiaotong UniversityMedical School, Xi'an 710061, The People's Republic of China.

出版信息

RNA. 2013 Jan;19(1):85-95. doi: 10.1261/rna.035295.112. Epub 2012 Nov 26.

DOI:10.1261/rna.035295.112
PMID:23185040
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3527729/
Abstract

The miR-302-367 cluster is specifically expressed in human embryonic stem cells and has been shown to convert human somatic cells into induced pluripotent stem cells. Here, we investigated the role of the miR-302-367 cluster in cervical carcinoma. The cluster was not endogenously expressed in cervical cancer cells, and its ectopic expression did not reprogram the cervical cancer cells to an embryonic stem cell-like state. However, ectopic expression of the miR-302-367 cluster in HeLa and SiHa cervical cancer cells inhibited cell proliferation and tumor formation by blocking the G1/S cell cycle transition. We identified a new cell cycle regulatory pathway in which the miR-302-367 cluster directly down-regulated both cyclin D1 and AKT1 and indirectly up-regulated p27(Kip1) and p21(Cip1), leading to the suppression of cervical cancer cell proliferation. Our findings suggest that the miR-302-367 cluster may be used as a therapeutic reagent for the treatment of cervical carcinoma.

摘要

miR-302-367 簇特异性表达于人类胚胎干细胞,并已被证明可将人类体细胞转化为诱导多能干细胞。在这里,我们研究了 miR-302-367 簇在宫颈癌中的作用。该簇在宫颈癌细胞中内源性表达,其异位表达并不能将宫颈癌细胞重新编程为胚胎干细胞样状态。然而,miR-302-367 簇在 HeLa 和 SiHa 宫颈癌细胞中的异位表达通过阻断 G1/S 细胞周期转换抑制细胞增殖和肿瘤形成。我们确定了一个新的细胞周期调控途径,其中 miR-302-367 簇直接下调细胞周期蛋白 D1 和 AKT1,并间接上调 p27(Kip1)和 p21(Cip1),从而抑制宫颈癌细胞的增殖。我们的研究结果表明,miR-302-367 簇可作为治疗宫颈癌的治疗试剂。