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