Dataset Information

Regulatory Mechanism of MicroRNA Expression in Cancer.

ABSTRACT: Altered gene expression is the primary molecular mechanism responsible for the pathological processes of human diseases, including cancer. MicroRNAs (miRNAs) are virtually involved at the post-transcriptional level and bind to 3' UTR of their target messenger RNA (mRNA) to suppress expression. Dysfunction of miRNAs disturbs expression of oncogenic or tumor-suppressive target genes, which is implicated in cancer pathogenesis. As such, a large number of miRNAs have been found to be downregulated or upregulated in human cancers and to function as oncomiRs or oncosuppressor miRs. Notably, the molecular mechanism underlying the dysregulation of miRNA expression in cancer has been recently uncovered. The genetic deletion or amplification and epigenetic methylation of miRNA genomic loci and the transcription factor-mediated regulation of primary miRNA often alter the landscape of miRNA expression in cancer. Dysregulation of the multiple processing steps in mature miRNA biogenesis can also cause alterations in miRNA expression in cancer. Detailed knowledge of the regulatory mechanism of miRNAs in cancer is essential for understanding its physiological role and the implications of cancer-associated dysfunction and dysregulation. In this review, we elucidate how miRNA expression is deregulated in cancer, paying particular attention to the cancer-associated transcriptional and post-transcriptional factors that execute miRNA programs.

SUBMITTER: Ali Syeda Z

PROVIDER: S-EPMC7084905 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature

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Regulatory Mechanism of MicroRNA Expression in Cancer.

Ali Syeda Zainab Z Langden Siu Semar Saratu' SSS Munkhzul Choijamts C Lee Mihye M Song Su Jung SJ

International journal of molecular sciences 20200303 5

Altered gene expression is the primary molecular mechanism responsible for the pathological processes of human diseases, including cancer. MicroRNAs (miRNAs) are virtually involved at the post-transcriptional level and bind to 3' UTR of their target messenger RNA (mRNA) to suppress expression. Dysfunction of miRNAs disturbs expression of oncogenic or tumor-suppressive target genes, which is implicated in cancer pathogenesis. As such, a large number of miRNAs have been found to be downregulated o ...[more]

PMID: 32138313

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Project description:Diabetic macular edema (DME) is the main cause of visual impairment in diabetic patients, but its pathogenesis remains unclear. The purpose of the present study was to analyze the expression of microRNA (miR)-155-5p in patients with DME and its regulatory mechanism. A total of 72 patients diagnosed with DME and 17 with idiopathic macular hole (MH) were recruited. Among samples from patients with DME, 45 were DME and 27 were refractory DME, whereas patients with idiopathic MH served as the control group. Optical coherence tomography and fundus photograph analysis revealed that part of the retina in the fundus of patients with DME was thickened, with macular edema occurring simultaneously. In refractory patients with DME, macular edema was associated with bleeding and a dark cavity between retinal layers. Through reverse transcription-quantitative PCR analysis, miR-155-5p was highly expressed in the aqueous humor (AH) and plasma of patients with DME compared with that in patients with MH, and this was even higher in the refractory DME group. Upon analyzing patient clinical data, the difference in miR-155-5p expression in the AH and plasma was positively associated with disease course, body mass index, fasting blood-glucose, glycated hemoglobin, proteinuria and glycosuria. The expression of miR-155-5p was not significantly different based on hemoglobin, intraocular pressure and sex. The aforementioned results indicate that miR-155-5p might promote the development of DME. To further study the molecular mechanism, human retinal microvascular endothelial cells (HRMECs) were cultured and treated with high glucose in vitro. The results showed that miR-155-5p expression was significantly upregulated in HRMECs induced by high glucose. After inhibiting the expression of miR-155-5p, cell proliferation, angiogenesis and VEGF protein levels were significantly downregulated, whereas miR-155-5p mimics had the opposite effect. In summary, miR-155-5p is closely associated with DME and is a potential target for refractory DME treatment.

Dataset Information

Regulatory Mechanism of MicroRNA Expression in Cancer.

Publications

Regulatory Mechanism of MicroRNA Expression in Cancer.

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