Adenosine A1 Receptor Antagonist Up-regulates Casp3 and Stimulates Apoptosis Rate in Breast Cancer Cell Line T47D

• Main Authors: Mohammad Zamani Rarani, Fahimeh Zamani Rarani, Ali Valiani, Zeinolabedin Shrifian Dastjerdi, Elias Kargar Abargouei, Ebrahim Eftekhar, Asghar Taheri Kafran, Majid Pourentezari, Malihe Saghebray, Farnoosh Razavi, Sanaz Hadizadeh, Mehdi Nikbakht Dastjerdi
• Format: Article
• Language: English
• Published: Hormozgan University of Medical Sciences 2020-03-01
• Series: Disease and Diagnosis
• Subjects: receptor; adenosine a1; apoptosis; genes; casp3; t47d cells
• Online Access: https://ddj.hums.ac.ir/PDF/A-10-165-1.pdf

Background: Adenosine receptor family, especially A1 type is-overexpressed in breast-derived tumor cells and the P53 gene is mutant in some of these cells while the casps gene is of wild type as well. The aim of this study was to evaluate the effect of the A1 receptor function on cell programmed death or proliferation, as well as the relationship between this receptor stimulation/inhibition and caspase 3 (casp3) expression in T47D cell line that has a mutant and non-functional P53 gene. Materials and Methods: The expression of casps3 was measured by real-time polymerase chain reaction and then flow cytometery and MTT assay were used to assess the apoptotic and proliferation cell rate after the treatment of T47D cells with specific agonist N6-cyclopentyladenosine (CPA) and antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) of this receptor 24, 48, and 72 hours after treatment. Result: Our results indicated that DPCPX significantly induces apoptosis in T47D cells and the rate of survival cell after the reduction of this treatment, especially 72 hours after treatment. Finally, the expression of casp3 was up-regulated by DPCPX treatment, especially in 72 hours while CPA treatment had opposite results (P>0.05). Conclusion: In general, DPCPX could up-regulate casp3 gene expression and subsequently increase the apoptosis rate in T47D cells with casp3 expression without the P53 gene interference. Therefore, adenosine A1 receptor antagonists may be introduced as anti-cancer agents.