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Genistin Represses the Proliferation and Angiogenesis While Accelerating the Apoptosis of Glioma Cells by Modulating
Xingyu Lan1, Zhihong Gui2, Taotao Chen3
1Department of Medical Education, Yunhe County People's Hospital, 323600 Lishui, Zhejiang, China.
Background:
Glioma is a tumor originating from glial cells and is the most common primary brain tumor. At present, the main treatment methods for glioma include surgical resection and radiotherapy and chemotherapy, but the treatment effect is not very ideal. Genistin (GS) inhibits breast cancer cell growth while promoting apoptosis, but its effect and detailed molecular mechanism on glioma are yet to be defined. In addition, forkhead box C1 (FOXC1) has been found to be involved in the growth, invasion, and angiogenesis processes of glioma cells.
Methods:
Human glioma cells in the Control, GS-6.25, GS-12.5, and GS25 (GS) groups were treated with 0, 6.25, 12.5, and 25 μM of Genistin, respectively, for 72 hours, and cells in the GS + NC (negative control) and GS + FOXC1 groups were transfected with negative control or forkhead box C1 (FOXC1) overexpression plasmids, respectively, prior to Genistin (25 μM) treatment for 72 hours. Next, the viability, proliferation, apoptosis, and angiogenesis of treated glioma cells were detected using Cell Counting Kit-8 (CCK-8), 5-ethynyl-2'deoxyuridine (EdU) proliferation, flow cytometry, and tube formation assays. Meanwhile, the half-maximal inhibitory concentration (IC50) of Genistin in the treated glioma cells was calculated. Afterwards, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot quantified the levels of FOXC1, Wnt1, Wnt3a, glycogen synthase kinase-3β (GSK3β), and phosphorylated GSK3β (p-GSK3β).
Results:
Genistin inhibited viability, proliferation, and angiogenesis while promoting the apoptosis of glioma cells (p < 0.05, p < 0.001). Also, Genistin decreased the levels of FOXC1, Wnt1, and Wnt3a while increasing p-GSK3β levels in glioma cells (p < 0.05, p < 0.01, p < 0.001). FOXC1 was up-regulated in glioma cells and tissues, and overexpressed FOXC1 overturned the effects of Genistin on the abovementioned factors in glioma cells (p < 0.05, p < 0.001).
Conclusions:
Genistin inhibits viability, proliferation, and angiogenesis while accelerating glioma cell apoptosis by modulating the FOXC1-mediated Wnt signaling pathway.
Insights
Genistin effectively inhibits glioma cell growth and promotes apoptosis by targeting the FOXC1-mediated Wnt signaling pathway. This study reveals a novel therapeutic strategy for glioma treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Glioma is the most common primary brain tumor with limited treatment efficacy.
- Genistin (GS) shows anti-cancer properties, but its mechanism in glioma is unclear.
- Forkhead box C1 (FOXC1) is implicated in glioma progression.
Purpose of the Study:
- To investigate the effects of Genistin on glioma cell viability, proliferation, apoptosis, and angiogenesis.
- To elucidate the molecular mechanism of Genistin in glioma, focusing on FOXC1 and Wnt signaling.
Main Methods:
- Glioma cells were treated with varying concentrations of Genistin.
- FOXC1 overexpression and control experiments were performed.
- Cell viability, proliferation, apoptosis, and angiogenesis were assessed.
- Gene and protein expression levels (FOXC1, Wnt pathway components) were quantified via qRT-PCR and Western blot.
Main Results:
- Genistin significantly inhibited glioma cell viability, proliferation, and angiogenesis, while promoting apoptosis.
- Genistin reduced FOXC1, Wnt1, and Wnt3a levels and increased p-GSK3β.
- FOXC1 overexpression counteracted the effects of Genistin.
Conclusions:
- Genistin demonstrates potent anti-glioma activity.
- The mechanism involves the modulation of the FOXC1-mediated Wnt signaling pathway.
- Genistin represents a promising therapeutic agent for glioma.
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