Dissertation
Dissertation > Medicine, health > Oncology > Hematopoietic and lymphoid neoplasms > Leukemia

The Study of the Apoptotic Mechanism of Multidrug Resistant Cell Line K562/A02 Induced by Tunicamycin

Author MaJunJie
Tutor JiChunYan
School Shandong University
Course Internal Medicine
Keywords apoptosis endoplasmic reticulum stress multidrug resistance tunicamycin Pgp
CLC R733.7
Type Master's thesis
Year 2010
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Objective: the emergence of multidrug resistance is the main reason for treatment failure and death in patients . Therefore, the study of the mechanism of multidrug resistance phenomenon , and accordingly design new targeted therapies , has an important significance for improving the therapeutic effect, prolonging patient survival . Therefore, we have to K562/A02 this representative multidrug resistant cell lines for the study, discusses the endoplasmic reticulum pathways vitro induced the K562/A02 apoptosis in effect and mechanism of tunicamycin (tunicamycin) . Methods: We first detected by MTT tunicamycin on of K562/A02 cell viability (IC50 values) ; then by flow cytometry tunicamycin treated K562/A02 cells Annexin V , Caspase -3 , 8 , 9, 12 , and other changes of protein expression were detected ; addition, we detect the concentration of tunicamycin treated K562/A02 intracellular epirubicin and Rhodamine123 MDY - 64 fluorescence intensity and the expression of P-gp explore the mechanism of tunicamycin - induced apoptosis . The Results: the tunicamycin 5.Oug/ml following K562 and K562/A02 cell inhibition rate of less than 30% , half inhibition (IC50 values ??) were 30.30ug/ml and 23.18ug/ml . Tunicamycin induced K562 and K562/A02 cell apoptosis , the role of tunicamycin K562/A02 cell expression of Caspase -12 9 cells increased , the average fluorescence intensity increased . Caspase-3, 8 expression did not change , the the tunicamycin role K562 and K562/A02 cells MDY-64 fluorescence intensity decreased . The tunicamycin 5.Oug/ml can lead to increased of K562/A02 drug sensitivity of the cells to doxorubicin , K562/A02 intracellular tunicamycin 5.Oug/ml role epirubicin , Rhodamine 123 volume increased significantly , but had no effect on the expression of P-gp . Conclusion Our results indicate that tunicamycin possible through injury K562/A02 cells endoplasmic reticulum , triggering endoplasmic reticulum stress , which K562/A02 multidrug resistant cell line by through endoplasmic reticulum ways to promote apoptosis .

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