Project description:This study aimed to identify differential expressed genes before and after tranfection with miR-215 and siPCAT1, using the 7721 liver cancer cell line as a model.
Project description:The whole human genome microarray was used for analysis of the differentially expressed genes in SMMC-7721 cells when exposed to 1 μM IMB5043 treatment for 24 h.
Project description:We performed a genome wide transcription profile analysis to determine the expression alterations between control and the POH1 siRNAs transfected SMMC-7721 cells The liver cancer cell line SMMC-7721 transfected with either the control or POH1 siRNAs were subjected to a genome wide transcription profile analysis through Human U133 Puls 2.0 (Affymetrix) microarray
Project description:HCC cell line SMMC-7721 were treatment with human recombinant artemin for 12 hours. Total RNA was extracted and the induced gene expression was analyzed.
Project description: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
Project description:To further development of our gene expression approach to microRNA-26a over-expression, we have employed whole mRNA microarray expression profiling as a discovery platform. SMMC-7721 cells at 70–80% confluence in 6-well plates were transfected using Lipofectamine 2000 (Invitrogen). Negative control mimics or miR-26a mimics (100nM) were transfected in each well. Cell extracts were prepared 48 h after transfection, total RNA was checked for a RIN number to inspect RNA integration by Affymetrix PrimeView™ Human Gene Expression Arrays. We used microarrays to detail the global programme of gene expression underlying miR-26a over-expression and identified distinct classes of up-regulated or down-regulated genes during this process.
Project description:HCC cell line SMMC-7721 were treatment with human recombinant artemin for 12 hours. Total RNA was extracted and the induced gene expression was analyzed. Analysis of gene expression induced by artemin treatment
