Parisa Zeinali, marie saghaeian, J. Asadi, S. Jafari
{"title":"High Dose of 3, 7-Dimethyl-1-Propargylxanthine Induces Cell Death in YM-1 and KYSE30 Cancer Cell Lines","authors":"Parisa Zeinali, marie saghaeian, J. Asadi, S. Jafari","doi":"10.52547/mlj.16.5.37","DOIUrl":null,"url":null,"abstract":"Background and objectives: Activation of adenosine A2a receptor has been shown to induce the growth and metastasis of cancer cells. The role of this receptor in esophageal cancer has not yet been determined. The present study aimed to investigate effects of an adenosine A2a receptor antagonist (3, 7-dimethyl-1-propargylxanthine) on growth of esophageal cancer cells. Methods: Real-time polymerase chain reaction was performed to evaluate mRNA expression of the A2a adenosine receptor in KYSE-30 and YM-1 esophageal cancer cell lines. Effects of the antagonist on viability of the cells were evaluated by MTT assay. Results: At low concentrations, the antagonist had no effect on cell viability. However, at concentrations ≥200 μM, the antagonist significantly reduced viability of both cell lines ( p <0.05). Conclusion: The results of this study indicate that the adenosine A2a receptor antagonist exerts inhibitory effects on KYSE30 and YM-1 cancer cells in a dose-dependent manner. Therefore, the use of this antagonist can be exploited as a therapeutic target for the treatment of esophageal cancer. at 60 °C. The obtained cycle thresholds were calculated by using the 2 -(ΔCT) method. Relative gene expression levels were calculated by defining a ratio between the amount of gene expression and the endogenous control. An analysis of the melting curve (60 °C to 95 °C increments of 0.3°C) was also performed to determine the melting temperature of specific amplicons and primer dimmers. All tests were performed in triplicate. Cells (10 4 cells per well) were seeded in 96-well plates. After 24 hours, the cells were treated with 20 µl of 3, 7-dimethyl-1-propargylxanthine (DMPX, Sigma, USA) as","PeriodicalId":32131,"journal":{"name":"Medical Laboratory Technology Journal","volume":"128 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medical Laboratory Technology Journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.52547/mlj.16.5.37","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
Background and objectives: Activation of adenosine A2a receptor has been shown to induce the growth and metastasis of cancer cells. The role of this receptor in esophageal cancer has not yet been determined. The present study aimed to investigate effects of an adenosine A2a receptor antagonist (3, 7-dimethyl-1-propargylxanthine) on growth of esophageal cancer cells. Methods: Real-time polymerase chain reaction was performed to evaluate mRNA expression of the A2a adenosine receptor in KYSE-30 and YM-1 esophageal cancer cell lines. Effects of the antagonist on viability of the cells were evaluated by MTT assay. Results: At low concentrations, the antagonist had no effect on cell viability. However, at concentrations ≥200 μM, the antagonist significantly reduced viability of both cell lines ( p <0.05). Conclusion: The results of this study indicate that the adenosine A2a receptor antagonist exerts inhibitory effects on KYSE30 and YM-1 cancer cells in a dose-dependent manner. Therefore, the use of this antagonist can be exploited as a therapeutic target for the treatment of esophageal cancer. at 60 °C. The obtained cycle thresholds were calculated by using the 2 -(ΔCT) method. Relative gene expression levels were calculated by defining a ratio between the amount of gene expression and the endogenous control. An analysis of the melting curve (60 °C to 95 °C increments of 0.3°C) was also performed to determine the melting temperature of specific amplicons and primer dimmers. All tests were performed in triplicate. Cells (10 4 cells per well) were seeded in 96-well plates. After 24 hours, the cells were treated with 20 µl of 3, 7-dimethyl-1-propargylxanthine (DMPX, Sigma, USA) as