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2000
Volume 15, Issue 3
  • ISSN: 1567-2026
  • E-ISSN: 1875-5739

Abstract

Background: Glioma is a type of tumor that starts in the glial cells of brain and spine. However, the underlying molecular mechanisms of miRNAs dysregulation in glioma initiation and progression is largely unclear. Objective: To further understand the molecular mechanism of miR-490-5P functions and how miR-490 regulated CCND1 function. Methods: The expression of miR-490-5P in glioma tissues and cells was measured by qRT-PCR and ISH. Cell transfection is responsible for miR-490-5P overexpression and knockdown. CCK-8 and clone formation assay are applicable to examine the capacity of glioma cells proliferation. Cell cycle analysis is used to test glioma cells cycle distribution with miR-490-5P overexpression or downregulation. Further, in vivo tumor exnograft studies are used to examine the effects of miR- 490-5P on glioma malignancy in vivo. Results: We found overexpression of miR-490 lead to glioma cells cycle arrest at G1 phase and decreased proliferation. Next-step functional assays showed miR-490 regulated CCND1 expression and manipulated giloma cells proliferation. Finally, negative regulation of miR-490 in CCND1 function was validated through in vivo nude mice tumorigenesis assay and IHC examination in glioma tissue. Conclusion: Overall, these results showed that epigenetic regulation of CCND1 via miR-490 was essential to glioma and provide a new insight into glioma diagnosis, treatment, prognosis and further translational investigations.

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/content/journals/cnr/10.2174/1567202615666180813130143
2018-08-01
2025-04-09
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/content/journals/cnr/10.2174/1567202615666180813130143
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  • Article Type:
    Research Article
Keyword(s): CCND1; Epigenetic modificaiton; G1 phase arrest; Glioma; glioma cells; MiR-490
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