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Activation of protease-activated receptor 2 reduces glioblastoma cell apoptosis.

Luo R, Wang X, Dong Y, Wang L, Tian C - J. Biomed. Sci. (2014)

Bottom Line: Factors regulating the apoptosis process are to be further understood.Exposure to tryptase, or the PAR2 active peptide, increased STAT3 phosphorylation in the radiated U87 cells, reduced U87 cell apoptosis, suppressed the expression of p53 in U87 cells.Activation of PAR2 can reduce the radiated U87 cell apoptosis via modulating the expression of p53.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Neurosurgery, Institute of Neurosurgery, Yichang Central People's Hospital & The First Clinical Medical College of Three Gorges University, Yichang, Hubei 443003, P,R, China. xiongweiwang4@163.com.

ABSTRACT

Background: The pathogenesis of glioma is unclear. The disturbance of the apoptosis process plays a critical role in glioma growth. Factors regulating the apoptosis process are to be further understood. This study aims to investigate the role of protease activated receptor-2 (PAR2) in regulation the apoptosis process in glioma cells.

Results: The results showed that U87 cells and human glioma tissue expressed PAR2. Exposure to tryptase, or the PAR2 active peptide, increased STAT3 phosphorylation in the radiated U87 cells, reduced U87 cell apoptosis, suppressed the expression of p53 in U87 cells.

Conclusions: Activation of PAR2 can reduce the radiated U87 cell apoptosis via modulating the expression of p53. The results implicate that PAR2 may be a novel therapeutic target in the treatment of glioma.

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Tryptase inhibits U87 cell apoptosis. The treatment of U87 cells is denoted above each dot plot panel. Radiation: U87 cells were treated with radiation (8Gy) in the culture. Dose of tryptase (control peptide and active peptide): 10 μg/ml. A, the dot plots indicat the frequency of PI+ U87 cells or/and Annexin V+ cells, which are summarized in B. PAR2d: U87 cells with the PAR2 gene knockdown. cshRNA: U87 cells treated with control shRNA. C, the PAR2 gene knockdown results. *, p < 0.01, compared with group A7 (mean ± SD). The data are from 3 separate experiments.
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Figure 2: Tryptase inhibits U87 cell apoptosis. The treatment of U87 cells is denoted above each dot plot panel. Radiation: U87 cells were treated with radiation (8Gy) in the culture. Dose of tryptase (control peptide and active peptide): 10 μg/ml. A, the dot plots indicat the frequency of PI+ U87 cells or/and Annexin V+ cells, which are summarized in B. PAR2d: U87 cells with the PAR2 gene knockdown. cshRNA: U87 cells treated with control shRNA. C, the PAR2 gene knockdown results. *, p < 0.01, compared with group A7 (mean ± SD). The data are from 3 separate experiments.

Mentions: Mast cells are associated with cancer growth[10]. Tryptase is one of the major chemical mediators of mast cells; it cleaves PAR2 to activate the PAR2-bearing cells. We postulate that tryptase activates U87 cells and influences the process of apoptosis induced by other factors such as radiation. Thus, we treated U87 cells with radiation in the presence or absence of tryptase or the PAR2 active peptide. As shown by flow cytometry data, about 4% apoptotic cells were detected in naïve U87 cells; after radiation, the apoptotic U87 cells reached 56%, which was abolished by the presence of tryptase or the PAR2 active peptide in the culture (Figure 2).


Activation of protease-activated receptor 2 reduces glioblastoma cell apoptosis.

Luo R, Wang X, Dong Y, Wang L, Tian C - J. Biomed. Sci. (2014)

Tryptase inhibits U87 cell apoptosis. The treatment of U87 cells is denoted above each dot plot panel. Radiation: U87 cells were treated with radiation (8Gy) in the culture. Dose of tryptase (control peptide and active peptide): 10 μg/ml. A, the dot plots indicat the frequency of PI+ U87 cells or/and Annexin V+ cells, which are summarized in B. PAR2d: U87 cells with the PAR2 gene knockdown. cshRNA: U87 cells treated with control shRNA. C, the PAR2 gene knockdown results. *, p < 0.01, compared with group A7 (mean ± SD). The data are from 3 separate experiments.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3974186&req=5

Figure 2: Tryptase inhibits U87 cell apoptosis. The treatment of U87 cells is denoted above each dot plot panel. Radiation: U87 cells were treated with radiation (8Gy) in the culture. Dose of tryptase (control peptide and active peptide): 10 μg/ml. A, the dot plots indicat the frequency of PI+ U87 cells or/and Annexin V+ cells, which are summarized in B. PAR2d: U87 cells with the PAR2 gene knockdown. cshRNA: U87 cells treated with control shRNA. C, the PAR2 gene knockdown results. *, p < 0.01, compared with group A7 (mean ± SD). The data are from 3 separate experiments.
Mentions: Mast cells are associated with cancer growth[10]. Tryptase is one of the major chemical mediators of mast cells; it cleaves PAR2 to activate the PAR2-bearing cells. We postulate that tryptase activates U87 cells and influences the process of apoptosis induced by other factors such as radiation. Thus, we treated U87 cells with radiation in the presence or absence of tryptase or the PAR2 active peptide. As shown by flow cytometry data, about 4% apoptotic cells were detected in naïve U87 cells; after radiation, the apoptotic U87 cells reached 56%, which was abolished by the presence of tryptase or the PAR2 active peptide in the culture (Figure 2).

Bottom Line: Factors regulating the apoptosis process are to be further understood.Exposure to tryptase, or the PAR2 active peptide, increased STAT3 phosphorylation in the radiated U87 cells, reduced U87 cell apoptosis, suppressed the expression of p53 in U87 cells.Activation of PAR2 can reduce the radiated U87 cell apoptosis via modulating the expression of p53.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Neurosurgery, Institute of Neurosurgery, Yichang Central People's Hospital & The First Clinical Medical College of Three Gorges University, Yichang, Hubei 443003, P,R, China. xiongweiwang4@163.com.

ABSTRACT

Background: The pathogenesis of glioma is unclear. The disturbance of the apoptosis process plays a critical role in glioma growth. Factors regulating the apoptosis process are to be further understood. This study aims to investigate the role of protease activated receptor-2 (PAR2) in regulation the apoptosis process in glioma cells.

Results: The results showed that U87 cells and human glioma tissue expressed PAR2. Exposure to tryptase, or the PAR2 active peptide, increased STAT3 phosphorylation in the radiated U87 cells, reduced U87 cell apoptosis, suppressed the expression of p53 in U87 cells.

Conclusions: Activation of PAR2 can reduce the radiated U87 cell apoptosis via modulating the expression of p53. The results implicate that PAR2 may be a novel therapeutic target in the treatment of glioma.

Show MeSH
Related in: MedlinePlus