Cargando…
Regulatory mechanism of miR-20a-5p expression in Cancer
MicroRNAs(miRNAs) are non-coding single-stranded RNA molecules encoded by endogenous genes with a length of about 22 nucleotides. The dysregulation of miRNAs has been proven to be one of the vital causes of cancer, which makes them a biomarker for cancer diagnosis and prognosis. Compared with surger...
Autores principales: | , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2022
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9110721/ https://www.ncbi.nlm.nih.gov/pubmed/35577802 http://dx.doi.org/10.1038/s41420-022-01005-5 |
Sumario: | MicroRNAs(miRNAs) are non-coding single-stranded RNA molecules encoded by endogenous genes with a length of about 22 nucleotides. The dysregulation of miRNAs has been proven to be one of the vital causes of cancer, which makes them a biomarker for cancer diagnosis and prognosis. Compared with surgery and chemotherapy, nucleic acid therapy targeting specific miRNAs is a promising candidate for cancer treatment. miR-20a-5p plays an anticancer role in high-incidence human cancers such as cervical cancer, breast cancer and leukemia, which is of great importance in the diagnosis of cancers. The up-regulation and down-regulation of miR-20a-5p offers a possible breakthrough for the treatment of cancers. In this paper, we aim to investigate the functional significance of miR-20a-5p in different cancers, reviewing the expression differences of miR-20a-5p in cancer, while systematically summarizing the changes of circRNA-miR-20a-5p networks, and probe how it promotes messenger RNA (mRNA) degradation or inhibits mRNA translation to regulate downstream gene expression. We’ve also summarized the biogenesis mechanism of miRNAs, and emphasized its role in cell proliferation, cell apoptosis and cell migration. On this basis, we believe that miR-20a-5p is a promising and effective marker for cancer diagnosis, prognosis and treatment. |
---|