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  1. Article ; Online: Investigation the Effect of Adenosine A1 Receptor Agonist and Antagonist on P53 Gene Expression, and Apoptosis Pathways and Rate in U87Mg Multiform Glioblastoma

    Fahimeh Zamani-Rarani / Zeinolabedin Shrifian-Dastjerdi / Ali Valiani / Mohammad Zamani-Rarani / Elias Kargar-Abargouei / Ebrahim Eftekhar / Majid Pourentezari / Javad Mohajer-Ansari

    مجله دانشکده پزشکی اصفهان, Vol 38, Iss 601, Pp 875-

    2021  Volume 881

    Abstract: Background: Improper prognosis in brain cancers requires new treatments. Using family of purinergic receptors with confirmed apoptotic effect can be beneficial. As the role of type A1 receptor in multiform glioblastoma in relation to the P53 gene and ... ...

    Abstract Background: Improper prognosis in brain cancers requires new treatments. Using family of purinergic receptors with confirmed apoptotic effect can be beneficial. As the role of type A1 receptor in multiform glioblastoma in relation to the P53 gene and apoptotic pathways is nor reported, we studied the role of agonist (N6-cyclopentyladenosine or CPA) and antagonist (8-cyclopentyl-1,3-dipropylxanthine or DPCPX) of this receptor on cell apoptosis and also expression of P53 genes and caspases 7, 8, and 9. Methods: In this study, MTT assay was used to investigate the rate of cellular proliferation, and flowcytometry method with annexin and Pi was also used to investigate early and late cell apoptosis. To evaluate the internal and external apoptotic pathways expression of P53 genes and caspases 7, 8, and 9, real-time reverse transcription polymerase chain reaction (real-time RT PCR) was used. Findings: The treatment of U87Mg cells with DPCPX increased the expression of P53 gene. Expression of caspase 7 as an executive caspase and caspase 9 as a caspase of the mitochondrial pathway of apoptosis increased, but no expression change was observed in the caspase 8 gene. Conclusion: The results of MTT and flowcytometry showed that DPCPX, in addition to suppressing cell proliferation, stimulated apoptosis in U87Mg cells. Inhibition of adenosine A1 receptors by stimulating the expression of genes involved in apoptotic pathways, especially mitochondrial pathway genes, suppressed cell proliferation and induced apoptosis in U87Mg cells.
    Keywords receptor ; adenosine a1 ; apoptosis ; p53 genes ; Medicine ; R ; Medicine (General) ; R5-920
    Subject code 570
    Language Persian
    Publishing date 2021-02-01T00:00:00Z
    Publisher Vesnu Publications
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Adenosine A1 Receptor Antagonist Up-regulates Casp3 and Stimulates Apoptosis Rate in Breast Cancer Cell Line T47D

    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

    Disease and Diagnosis, Vol 9, Iss 1, Pp 14-

    2020  Volume 20

    Abstract: 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 ... ...

    Abstract 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.
    Keywords receptor ; adenosine a1 ; apoptosis ; genes ; casp3 ; t47d cells ; Medicine ; R
    Subject code 616 ; 610
    Language English
    Publishing date 2020-03-01T00:00:00Z
    Publisher Hormozgan University of Medical Sciences
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

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