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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]
Many miRNAs can directly target and inhibit cell cycle genes to control cell proliferation. A new strategy for tumor treatment is to inhibit tumor cell proliferation by repairing the defective miRNA pathway in tumors. [169] Cancer is caused by the accumulation of mutations from either DNA damage or uncorrected errors in DNA replication. [170]
The Let-7 microRNA precursor gives rise to let-7, a microRNA (miRNA) involved in control of stem-cell division and differentiation. [1] let-7, short for "lethal-7", was discovered along with the miRNA lin-4 in a study of developmental timing in C. elegans, [2] making these miRNAs the first ever discovered.
Inhibition of miRNA-26a increases gene expression of SMAD-1 and SMAD-4, while overexpression inhibits SMAD-1. [5] Hepatocellular carcinoma miR-26a has been found to induce cell cycle arrest at the G 1 phase in human hepatocellular carcinoma cells, in part through direct downregulation of cyclin D2 and cyclin E2.
Carcinogenesis is a gradual process, involving multiple genetic mutations, thus every patient with malignancy presents with a heterogeneous population of cells. The fact that mir-16 microRNA loss is observed in a large proportion of cells indicates the change occurred early in cancer development [23] and a target for therapeutic intervention.
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.
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.
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 ...