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کاربرد نوع شرط:
- جایگاه : پژوهشی
- مجله: Asian Pacific Journal of Cancer Prevention
- نوع مقاله: Journal Article
- کلمات کلیدی: Apoptosis,Acute Lymphoblastic Leukemia,DNA Methylation,Prednisolone,Methylation Specific PCR (MSP)
- چکیده:
- چکیده انگلیسی: Objective: one of the main mechanisms in which cancer cells are resistant to chemotherapy drugs and therapeutic strategies is resistance to apoptosis due to these anticancer factors. Regulating the expression of genes through epigenetics, especially regulation through methylation, is one of the key aspects of regulating gene expression and the function of genes, which is also regulated by the pathways regulating the pathway of apoptosis. The epigenetic regulatory phenomenon in cancer cells can undergo a change in regulation and induces resistance to apoptosis against chemotherapy and anticancer factors. The purpose of the present scrutiny was defined to probe the effect of subtoxic prednisolone dose on the level of promoter methylation and gene expression of BAX and BCL2 in the CCRF-CEM cells. Methods: The treated cells by prednisolone, cultured in RPMI 1640 medium in standard condition. Alteration in promoter DNA methylation was analyzed by use of methylation specific-PCR (MSP) technique after the defined intervened time of Prednisolone treatment with a subtoxic dose. Results: Prednisolone can induce apoptosis via alteration in BAX and BCL2 genes, based on our previous scrutiny. This essay shows no varies in the Pattern of DNA methylation of examined genes; however, prednisolone changes the expression of examined genes. Conclusion: Lack of alteration through prednisolone treatment in DNA methylation template of BAX and BCL2 genes make this possible that Prednisolone affects apoptotic gene expression via different pathways, which need more research to be done about it.
- انتشار مقاله: 23-07-1398
- نویسندگان: Saiedeh Ganbarjeddi,Ako Azimi,Milad Zadi Heydarabad,Maryam Hemmatzadeh,Shahin Mohammadi,Reza Mousavi Ardehaie,Majid Zamani,Sina Baharaghdam,Sajjad Esmaeili,Amin Ghasemi
- مشاهده
- جایگاه : پژوهشی
- مجله: Asian Pacific Journal of Cancer Prevention
- نوع مقاله: Journal Article
- کلمات کلیدی: Acute Lymphoblastic Leukemia,Protein expression,Resveratrol,Prednisolone,MDR1 gene
- چکیده:
- چکیده انگلیسی: Objective: Chemotherapy is the most widely recognized technique to regard leukemia and also different sorts of
human tumors. In any case, tranquilize protection has stayed as the primary test against the adequacy of medications.
Besides, having different unfriendly impacts, chemotherapy drugs are getting to be traded by characteristic modalities for
growth treatment. In such manner, natural segments, for example, resveratrol and prednisolone have been recognized to
sharpen the leukemic cells to modified cell demise through an arrangement of complex procedures. In this investigation,
we have analyzed effect of 15, 50 and 100μM of resveratrol and 700μM of prednisolone on the human multidrug
protection quality 1 (MDR1) as a notable marker for cell sedate protection. We assessed the impact of resveratrol and
prednisolone on MDR1 protein expression in the CCRF-CEM cell line as an agent for intense lymphoblastic leukemia.
The investigation was planned to clear up whether. Materials and methods: CCRF-CEM cells linage get under
drug treatment with use of resveratrol and prednisolone. Western blot use at 24 and 48 hours with different doses of
resveratrol and prednisolone to analysis of MDR1 expression changes. Results: Effect of 15, 50, and 100 micro molar
of resveratrol and 700 micro molars of prednisolone on CCRF-CEM cells led to the MDR1 decrease. Western blot use
for evaluation of MDR1 protein expression changes. Conclusion: In the present study, we observed that resveratrol
and prednisolone, with a dose-dependent effect, can reduce the expression of the MDR1 protein. This reduction of
expression demonstrates that resveratrol and prednisolone can overcome to drug resistance created by MDR1.- انتشار مقاله: 14-07-1397
- نویسندگان: Mehdi Talebi,Sina Bahar Aghdam,Ako Azimi,Hamed Mohammadi,Somayyeh Karimi Yonjali,Maryam Asariha,Milad Zadi Heydarabad
- مشاهده