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Using a lineage tracing approach followed by Fluorescent-activated cell sorting, miRNA profiling of the FoxD1-derived cells not only comprehensively defined the transcriptional landscape of miRNAs that are critical for vascular development, but also identified key miRNAs that are likely to modulate the renal phenotype in its absence. These ...
miR-15a/16-1 deletion has been shown to accelerate the proliferation of both human and mouse B-cells through modulation of the expression of genes controlling cell cycle progression. [5] Studies have found the miR-15a/16-1 microRNA cluster to function as a tumour suppressor, with the oncogene BCL2 as its target. [6]
The RNase III Dicer is a critical member of RISC that initiates the RNA interference process by producing double-stranded siRNA or single-stranded miRNA. Enzymatic cleavage of dsRNA within the cell produces the short siRNA fragments of 21-23 nucleotides in length with a two-nucleotide 3' overhang.
p53-deficient human gastric cancer cells, restoration of functional miR-34 inhibits cell growth and induces chemosensitization and apoptosis, indicating that miR-34 may restore p53 function. Restoration of miR-34 inhibits tumorsphere formation and growth, which is reported to be correlated to the self-renewal of cancer stem cells.
A miRNA is expressed from a much longer RNA-coding gene as a primary transcript known as a pri-miRNA which is processed, in the cell nucleus, to a 70-nucleotide stem-loop structure called a pre-miRNA by the microprocessor complex. This complex consists of an RNase III enzyme called Drosha and a dsRNA-binding protein DGCR8.
While miR-125a acts as an oncogenic miRNA in non-blood cancers, its oncogenic functions have been described in cervical cancer, colorectal cancer, nasopharyngeal carcinoma and esophageal carcinomas. [5] On the other hand, high expression of miR-125b was shown to decrease cell proliferation and induces apoptosis.
This appears counter-intuitive firstly because there is no obvious source for miRNA production or maintenance in blood plasma, and secondly because there seems to be an inverse relationship between leukaemia cell miR-92 levels and blood plasma miR-92 levels in patients with the disease. 91 miRNAs are present in human plasma [10] and it has been ...
The paralogous miRNA gene clusters that give rise to miR-17 family microRNAs (miR-17~92, miR-106a~363, and miR-106b~25) have been implicated in a wide variety of malignancies and are sometimes referred to as oncomirs. [4] The oncogenic potential of these non-protein encoding genes was first identified in mouse viral tumorigenesis screens.