Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0017636 (
glioblastoma
)
18,345
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Glioblastoma
(
GBM
) is the most common malignant primary tumor in the human central nervous system. The present study aimed to explore the molecular mechanism by which microRNA (miR)-181a-5p targets the
F-box protein 11
(
FBXO11
) in glioma cells to inhibit cell proliferation and invasion. Reverse transcription-quantitative (RT-q)PCR was performed to detect the expression levels of miR-181a-5p in U251TR cells, U251 cells, primary
GBM
tissues and relapsed
GBM
tissues in order to determine the association between miR-181a-5p and the chemoresistance of
GBM
cells. The expression levels of miR-181a-5p in
GBM
cells were modulated via transfecting miR-181a-5p mimics and inhibitors. Cell Counting Kit-8 assays were undertaken to assess the effects of miR-181a-5p on drug sensitivity and proliferation of
GBM
cells. Wound healing assays were performed to examine the effects of miR-181a-5p on the migratory ability of
GBM
cells. Furthermore, the effects of miR-181a-5p on the invasive ability of
GBM
cells were analyzed using an
in vitro
invasion assay. Flow cytometry analysis was carried out to determine whether overexpression of miR-181a-5p can promote the apoptotic rate of
GBM
cells. RT-qPCR and western blotting were employed to detect the effects of miR-181a-5p on mRNA and protein expression of FBX011. miR-181a-5p exhibited low expression in resistant
GBM
cell lines and recurrent tumor tissues. Dual-luciferase reporter assays were utilized to detect luciferase activity to verify the targeted regulatory association between miR-181a-5p and
FBXO11
. Upregulation of miR-181a-5p promoted the sensitivity of
GBM
cells to temozolomide (TMZ), increased the apoptotic rate of
GBM
cells and significantly inhibited the invasive and migratory capacities of
GBM
cells. In drug-resistant glioma cells, compared with the miR-negative control group and the blank group, the expression of miR-181a-5p was significantly upregulated (P<0.01), while the expression of FBXO11 protein was downregulated. miR-181a-5p increased the sensitivity of
GBM
cells to TMZ. miR-181a-5p significantly inhibited the migratory and invasive capacities of
GBM
cells. miR-181a-5p may become a novel effective target for the treatment of
GBM
. The results of dual-luciferase reporter assays indicated that miR-181a-5p could target the 3'-untranslated region of
FBXO11
. The underlying mechanism may be targeted inhibition of
FBXO11
gene expression, or may be associated with apoptosis.
...
PMID:miR-181a-5p inhibits the proliferation and invasion of drug-resistant glioblastoma cells by targeting F-box protein 11 expression. 3296 57
