| GeneLibs

题目:: Coordinated regulation of cell cycle transcripts by p53-inducible microRNAs, miR -192 and -215
ID:
状态:: 发布时间June 24, 2010 , 更新时间 May 4, 2014 , 提交时间 Oct. 6, 2008,
物种:: Homo sapiens
摘要:: Cell cycle arrest in response to DNA damage is an important anti-tumorigenic mechanism. microRNAs (miRNAs) were shown recently to play key regulatory roles in cell cycle progression. For example, miR-34a is induced in response to p53 activation and mediates G1 arrest by down-regulating multiple cell cycle-related transcripts. Here we show that genotoxic stress promotes the p53-dependent up-regulation of the homologous miRNAs, miR -192 and miR-215. Like miR-34a, activation of miR-192/215 induces cell cycle arrest suggesting that multiple microRNA families operate in the p53 network. Furthermore, we define a downstream gene expression signature for miR-192/215 expression that includes a number of transcripts that regulate G1 and G2 checkpoints. Of these transcripts, 18 transcripts are direct targets of miR-192/215 and the observed cell cycle arrest likely results from a cooperative effect among the modulations of these genes by the miRNAs. Our results demonstrating a role for miR-192/215 in cell proliferation combined with recent observations that these miRNAs are under-expressed in primary cancers support the idea that miR-192 and miR-215 function as tumor-suppressors. Description: Transfection of siRNA luc, miR-192 or miR-215 into HCT116 Dicerex5, compared to mock-transfected cells, with mRNA expression profiled at 10h and 24h post-transfection. Species: Human Tissue: HCT116 Dicerex5 cell line (tissue of origin = human colorectal carcinoma); this cell line is hypomorphic for Dicer gene function. Dye-swap: no Negative control: siRNA luc Replicates per each timepoint: no
实验种类:: transcription profiling by array
样本量:: 12
实验设计:
: 无设计数据
数据号:: E-GEOD-13105, GSE13105
数据状态:: 无法自动分析，您可以尝试手动分析数据。

实验库数据相关信息

DataTable pData

联系方式

微信公众号

实验库 数据相关信息

DataTable pData

联系方式

微信公众号

实验库数据相关信息