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Boshra Haghi, Marie Saghaeian Jazi, Mahdi Zarie, Ayyoob Khosravi, Mahboubeh Tajaldini, Jahanbakhsh Asadi,
Volume 15, Issue 2 (Mar-Apr 2021)
Abstract

Background and objectives: Docetaxel is a chemotherapeutic agent commonly used for treatment of many cancers, including esophageal squamous cell carcinoma. Docetaxel induces G2/M phase cell cycle arrest and ultimately cell death. In this study, we aimed to assess the effects of docetaxel on YM1 cells considering exposure time and dose.
Methods: After calculating the doubling time of YM1 cells, the anti-proliferative effect of different concentrations of docetaxel () [A1]  after 24, 48 and 72 hours was assessed by the standard colorimetric assay. In addition, the effect of docetaxel on cell cycle was evaluated by flow cytometry.
Results: The results showed that docetaxel toxicity was not significant until 24 hours at the tested concentrations (P>0.05). In addition, the effect of docetaxel on the cells was time-dependent at all tested concentrations. Overall, the duration of exposure to docetaxel had more significant role in docetaxel toxicity in YM1 cells compared to concentration.
Conclusion: Our findings suggest that the cytotoxicity of docetaxel on YM1 cells is time-dependent.

 [A1]Please write the concentrations

Parisa Zeinali, Marie Saghaeian, Jahanbakhsh Asadi, Seyyed Mehdi Jafari,
Volume 16, Issue 5 (Sep-Oct 2022)
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.

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