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MiRNAs: regulators of human disease
MicroRNAs (miRNAs) represent the mediators of important leading biological functions of molecular pathways in humans. They are a class of very small, non-coding RNAs; their function is the balance of the protein levels at the post-transcriptional stage. They are implicated in molecular processes and...
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Published in: | European journal of gynaecological oncology 2016, Vol.37 (6), p.759-765 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Citations: | Items that cite this one |
Online Access: | Get full text |
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Summary: | MicroRNAs (miRNAs) represent the mediators of important leading biological functions of molecular pathways in humans. They are a class of very small, non-coding RNAs; their function is the balance of the protein levels at the post-transcriptional stage. They are implicated in molecular processes and diseases, including diabetes, metabolism, autoimmune diseases, angiogenesis and tumorigenesis, and female fertility, exhibiting an altered expression profile. Any process taking place in the human organism is intertwined by miRNAs. MiRNAs have an impact on the biochemistry of pathways of the invisible molecular world. They circulate in a stable chemical configuration in body fluids (tears, serum, plasma, amniotic fluid, ascetic fluid, urine) with their molecular sequence specificity remaining unchanged. Their indisputable molecular stability ranks them as extremely vigorous potential markers in human disease. MiRNAs demonstrate a specific expressive signature, representative of the tissue specificity and the clinical staging. The shift on the concentration and expression of a miRNA reflects the course of a disease. MiRNAs may operate as oncogenes (tumor growth) or tumor suppressor (tumor reduction) genes in cancer pathways. In malignant disease, proliferation, maintenance, and progression of cancer cells is induced by the stimulation of the oncogenes or complete deactivation of the tumor suppressor gene activity. |
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ISSN: | 0392-2936 |
DOI: | 10.12892/ejgo3184.2016 |