Related Experiment Video
Updated: Feb 5, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
The function of MMP-28/TGF-β induced cell apoptosis in human glioma cells
Xuepeng Wang1, Xi Chen2, Lin Sun3
1Department of Neurosurgery, Affiliated Hospital of Beihua University, Jilin 132000, P.R. China.
Abstract:
The aim of the present study was to assess the expression status of matrix metalloproteinase (MMP)-28 and to investigate its molecular mechanisms in glioma cells. MicroRNA (miRNA) reverse transcription-quantitative polymerase chain reaction was used to analyze the expression of MMP-28 and transforming growth factor (TGF)-β expression in glioma patients and healthy volunteers. MTT and Transwell assays were conducted to determine cell growth and metastasis, respectively. Annexin V/propidium iodide staining was also employed to measure cell apoptosis. MMP-28 and TGF-β protein expression were measured using western Blot analysis. The results indicated that MMP-28 and TGF-β expression was downregulated in glioma patients, when compared with the normal group. Overall survival and disease-free survival of patients with a low expression of MMP-28 were lower than those with high MMP-28 expression. Overexpression of MMP-28 induced TGF-β protein expression, while downregulation of MMP-28 suppressed TGF-β protein expression in glioma cell. The downregulation of MMP-28 reduced the cell growth and apoptosis of glioma cell via the suppression of TGF-β. By contrast, upregulation of MMP-28 induced cell growth and reduced the apoptosis of glioma cells by activating TGF-β. In addition, the TGF-β inhibitor attenuated the effects of MMP-28 in glioma cells. Collectively, the results indicated that MMP-28 was able to induce TGF-β in human glioma cells.
Insights
Matrix metalloproteinase (MMP)-28 is downregulated in glioma and influences tumor growth and apoptosis by inducing transforming growth factor (TGF)-β. Low MMP-28 expression correlates with poorer patient survival in glioma.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Glioma is a primary brain tumor with complex molecular mechanisms.
- Matrix metalloproteinase (MMP)-28 is a potential regulator in cancer, but its role in glioma is not fully understood.
- Transforming growth factor (TGF)-β signaling is implicated in glioma progression.
Purpose of the Study:
- To investigate the expression status of MMP-28 in glioma.
- To elucidate the molecular mechanisms of MMP-28 in glioma cells, focusing on its relationship with TGF-β.
- To assess the impact of MMP-28 on glioma cell growth, apoptosis, and metastasis.
Main Methods:
- Quantitative polymerase chain reaction (qPCR) for MMP-28 and TGF-β mRNA expression.
- MTT and Transwell assays for cell proliferation and migration.
- Annexin V/propidium iodide staining for apoptosis assessment.
- Western blot analysis for MMP-28 and TGF-β protein levels.
Main Results:
- MMP-28 and TGF-β expression were significantly downregulated in glioma tissues compared to normal tissues.
- Lower MMP-28 expression was associated with reduced overall survival and disease-free survival in glioma patients.
- MMP-28 overexpression upregulated TGF-β, promoting glioma cell growth and inhibiting apoptosis.
- MMP-28 downregulation suppressed TGF-β, leading to decreased cell growth and increased apoptosis.
- Inhibition of TGF-β attenuated the effects of MMP-28 on glioma cells.
Conclusions:
- MMP-28 is downregulated in human glioma and acts as an inducer of TGF-β.
- MMP-28/TGF-β signaling pathway plays a crucial role in regulating glioma cell proliferation and apoptosis.
- MMP-28 may serve as a potential therapeutic target or prognostic biomarker for glioma.
Related Concept Videos
TGF - β Signaling Pathway
Induced Pluripotent Stem Cells
Induced Pluripotent Stem Cells
Somatic...
Apoptosis
Cell Specific Gene Expression
T Cell Types and Functions
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...

