Abstract
This study purposed to explore the correlation between miR‐129‐5p and TGIF2 and their impacts on glioma cell progression. Differentially expressed miRNA was screened through microarray analysis. MiR‐129‐5p expression levels in glioma tissues and cells were measured by qRT‐PCR. CCK‐8 assay, flow cytometer, transwell assay and wound‐healing assay were employed to detect cell proliferation, apoptosis and cycle, invasiveness and migration, respectively. Dual‐luciferase reporting assay was performed to confirm the targeted relationship between miR‐129‐5p and TGIF2. The effects of TGIF2 expression on cell biological functions were also investigated using the indicated methods. Tumour xenograft was applied to explore the impact of miR‐129‐5p on tumorigenesis in vivo. MiR‐129‐5p expression was down‐regulated in both glioma tissues and glioma cells, while TGIF2 expression was aberrantly higher than normal level. Dual‐luciferase reporter assay validated the targeting relation between miR‐129‐5p and TGIF2. Overexpression of miR‐129‐5p or down‐regulation of TGIF2 inhibited the proliferation, invasion and migration capacity of glioma cells U87 and U251, and meanwhile blocked the cell cycle as well as induced cell apoptosis. MiR‐129‐5p overexpression repressed the tumour development in vivo. MiR‐129‐5p and TGIF2 had opposite biological functions in glioma cells. MiR‐129‐5p could inhibit glioma cell progression by targeting TGIF2, shining light for the development of target treatment for glioma.
Highlights
Glioma is the most untreatable tumour of the central nervous system with significant mortality and poor survival rate.[1]
Flow cytometric analysis showed that cell apoptosis rate was notably higher in miR-129-5p overexpression group while was lower in antimiR-129-5p group compared with the mock group, indicating that overexpression of miR-129-5p induced the apoptosis of glioma cells U87 and U251 (P < .05, Figure 3A)
The results demonstrated that overexpression of TGIF2 decreased cell apoptosis rate, while the inhibition of TGIF2 accelerated the apoptosis of glioma cells, which was impeded by anti-miR-129-5p (P < .05, Figure 7A)
Summary
Glioma is the most untreatable tumour of the central nervous system with significant mortality and poor survival rate.[1]. Zhou et al reported that miR-224 could drive colorectal cancer cell proliferation by targeting SMAD4.5 MiR-203 was reported to suppress tumour growth and metastasis of. Non-small cell lung cancer by down-regulating RGS17.6 Previous studies have provided some novel perspectives for the therapy of human glioma based on the modulating mechanism of miRNAs. For instance, miR-145 could induce glioma cell apoptosis by targeting BNIP3 and Notch signalling,[7] while miR-543 could suppress glioma in vitro and in vivo.[8]. We investigated the relationship between miR-129-5p and TGIF2 and explored their impacts on glioma cell progression
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