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Updated: Aug 2, 2025
Characterization of Functionally Associated miRNAs in Glioblastoma and their Engineering into Artificial Clusters for Gene Therapy
Published on: October 4, 2019
Scutellarin inhibits glioma cell proliferation by up-regulating miR-15a expression
Jiangfeng Du1,2, Ji Li2, Jianjun Tan3
1Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University No. 1 Medical College Road, Yuzhong District, Chongqing 400016, China.
Objective:
To investigate the effect of scutellarin on the proliferation of glioma cells through microRNA (miR)-15a.
Methods:
Human glioma cell line T98G was cultured in vitro and divided into control group (without treatment), scutellarin group (with 10, 20, 40, 80, 160 μg/mL scutellarin, respectively), miR-15a negative control group (transfected with negative control-miR-15a + 80 μg/mL scutellarin) and miR-15a inhibitor group (transfected with miR-15a siRNA + 80 μg/mL scutellarin). The proliferation of T98G cells was detected by cell counting kit-8 (CCK-8), and the expression of miR-15a in T98G cells was detected by real-time fluorescence quantitative PCR (qRT-PCR). The apoptosis of T98G cells was assessed by flow cytometry, and the invasion of T98G cells was compared by Transwell method. The levels of proliferating cell nuclear antigen (PCNA), Bcl-2 related X protein (Bax) and matrix metalloproteinase 9 (MMP-9) in T98G cells were detected by Western blot (WB).
Results:
Compared with that in the control group, the OD value of T98G cells in scutellarin group was significantly lower (P<0.05), with the increase of scutellarin concentration, the OD value of T98G cells decreased in turn, and 80 μg/mL was used as the optimal concentration of scutellarin to treat T98G cells for subsequent experiments. Compared with those in the control group, the miR-15a expression, apoptosis rate and Bax protein expression in T98G cells of scutellarin group were higher (P<0.05), and the OD value, number of invasive cells, PCNA and MMP-9 protein levels were lower (P<0.05). Compared with scutellarin group and miR-15a negative control group, the miR-15a expression, apoptosis rate and Bax protein expression in T98G cells of miR-15a inhibitor group were lower (P<0.05), and the OD value, number of invasive cells, PCNA and MMP-9 protein levels were higher (P<0.05).
Conclusions:
Scutellarin can inhibit the proliferation, invasion and induce the apoptosis of glioma cells, which may be mediated by up-regulating the expression of miR-15a.
Insights
Scutellarin inhibits glioma cell proliferation and invasion by up-regulating microRNA (miR)-15a. This natural compound also induces apoptosis, offering potential therapeutic benefits for glioma treatment.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Glioblastoma (GBM) is an aggressive brain tumor with limited treatment options.
- MicroRNAs (miRNAs) play crucial roles in cancer development and progression.
- Scutellarin is a natural flavonoid with potential anti-cancer properties.
Purpose of the Study:
- To investigate the anti-cancer effects of scutellarin on glioma cells.
- To elucidate the role of microRNA (miR)-15a in scutellarin-mediated glioma cell inhibition.
Main Methods:
- Human glioma T98G cells were treated with varying concentrations of scutellarin.
- Cell proliferation was assessed using CCK-8 assays.
- Apoptosis, invasion, and protein expression (PCNA, Bax, MMP-9) were evaluated using flow cytometry, Transwell assays, and Western blotting, respectively.
- miR-15a expression levels were quantified using qRT-PCR.
Main Results:
- Scutellarin significantly inhibited glioma cell proliferation and invasion in a dose-dependent manner.
- Scutellarin treatment led to increased miR-15a expression and apoptosis.
- Inhibition of miR-15a reversed the anti-proliferative and anti-invasive effects of scutellarin.
Conclusions:
- Scutellarin exhibits potent anti-glioma activity by inhibiting proliferation and invasion.
- The mechanism involves the up-regulation of miR-15a, leading to increased apoptosis.
- Scutellarin represents a promising therapeutic agent for glioma treatment.
