We compared gene expression profiles between asymptomatic and symptomatic atherosclerotic plaques from the same patient. This was accomplished by analyzing carotid plaques from four patients with bilateral high-grade carotid artery stenoses one being symptomatic (TIA or stroke) and the other asymptomatic.
Microarray analysis reveals overexpression of CD163 and HO-1 in symptomatic carotid plaques.
Sex, Age, Specimen part, Disease, Disease stage, Subject, Time
View SamplesGene expression profiling of supraclavicular brown, interscapular brown, inguinal white, and epididymal white adipose tissues from C57BL/6 male mice was performed by RNA-sequencing. Overall design: Total of 12 RNA samples (3 RNA samples from each adipose tissue type) from adipose tissues were used for RNA-sequencing analysis.
Identification and characterization of a supraclavicular brown adipose tissue in mice.
Sex, Specimen part, Cell line, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A set of NF-κB-regulated microRNAs induces acquired TRAIL resistance in lung cancer.
Cell line
View SamplesWe generated H460 cells with acquired TRAIL resistance by exposing the parental sentisitve cells to subtoxic concentrations of TRAIL for 6 months. Then we compared the gene expression profile of the sensitive versus the resistant cells.
A set of NF-κB-regulated microRNAs induces acquired TRAIL resistance in lung cancer.
Cell line
View SamplesNumerous studies have described the altered expression and the causal role of miRNAs in human cancer. However, to date efforts to modulate miRNA levels for therapeutic purposes have been challenging to implement. Here, we find that Nucleolin (NCL), a major nucleolar protein, post-transcriptionally regulates the expression of a specific subset of miRNAs, including miR-21, miR-221, miR-222, and miR-103, causally involved in breast cancer initiation, progression and drug-resistance. We also show that NCL is commonly overexpressed in human breast tumors, and its expression correlates with that of NCL-dependent miRNAs. Finally, this study indicates that NCL-binding guanosine-rich aptamers affect the levels of NCL-dependent miRNAs and their target genes, reducing breast cancer cell aggressiveness, both in vitro and in vivo. These findings illuminate a path to novel therapeutic approaches based on NCL-targeting aptamers for the modulation of miRNA expression in the treatment of breast cancer.
In vivo NCL targeting affects breast cancer aggressiveness through miRNA regulation.
Cell line
View SamplesCancer metastasis is a multistep processes based on reciprocal interanctions between tumor cells and their surroundings. From this experiments, we aim to investigate the contribution of TUSC3 deficency in lung cancer metastasis.
miRNA-mediated TUSC3 deficiency enhances UPR and ERAD to promote metastatic potential of NSCLC.
Cell line
View Samples