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학회지, 권호수 : EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE
JNK1/2 Activation by an Extract from the Roots of Morus alba L. Reduces the Viability of Multidrug-Resistant MCF-7/Dox Cells by Inhibiting YB-1-Dependent MDR1 Expression
Youn Kyung Choi, Sung-Gook Cho, Hyeong Sim Choi, Sang-MiWoo, Yee Jin Yun, Yong Cheol Shin, Seong-Gyu
    ABSTRACT
Cancer cells acquire anticancer drug resistance during chemotherapy, which aggravates cancer disease. MDR1 encoded from multidrug resistance gene 1 mainly causes multidrug resistance phenotypes of different cancer cells. In this study, we demonstrate that JNK1/2 activation by an extract from the root of Morus alba L. (White mulberry) reduces doxorubicin-resistant MCF-7/Dox cell viability by inhibiting YB-1 regulation of MDR1 gene expression. When MCF-7 or MCF-7/Dox cells, where MDR1 is highly expressed were treated with an extract fromroots or leaves of Morus alba L., respectively, the root extract fromthemulberry (REM) but not the leaf extract (LEM) reduced cell viabilities of both MCF-7 and MCF-7/Dox cells, which was enhanced by cotreatment with doxorubicin. REM but not LEM further inhibited YB-1 nuclear translocation and its regulation of MDR1 gene expression. Moreover, REMpromoted phosphorylation of c-Jun NH2-terminal kinase 1/2 (JNK1/2) and JNK1/2 inhibitor, SP600125 and rescued REM inhibition of bothMDR1 expression and viabilities inMCF-7/Dox cells. Consistently, overexpression of JNK1, c-Jun, or c-Fos inhibited YB-1-dependentMDR1 expression and reduced viabilities inMCF-7/Dox cells. In conclusion, our data indicate that REMactivated JNK-cJun/c-Fos pathway decreases the viability ofMCF-7/Dox cells by inhibiting YB-1- dependentMDR1 gene expression. Thus, we suggest that REM may be useful for treating multidrug-resistant cancer cells.

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