NDLI: Downregulation of MDR1 Gene by Cepharanthine Hydrochloride Is Related to the Activation of c-Jun/JNK in K562/ADR Cells

Content Provider	PubMed Central
Author	Han, Li Wang, Yafeng Guo, Xiaojuan Zhou, Yubing Zhang, Jingmin Wang, Ning Jiang, Jinhua Ma, Fang Wang, Qingduan
Copyright Year	2014
Abstract	The purpose of the study was to determine the signal transduction mechanism of cepharanthine hydrochloride (CH) on reversing tumor multidrug resistance. RT-PCR and Western blot analysis were used to determine the effects of CH on the expression of MDR1 mRNA and P-glycoprotein in K562/ADR cells when CH was used alone and combined with SP600125, a JNK inhibitor, to explore the effects of CH on JNK pathway. Western blot analysis was used to determine the effects of CH on c-Jun protein expression and phosphorylation, to explore the regulating effects of CH on c-Jun and phosphorylated c-Jun (p-c-Jun) proteins. Our results showed that the inhibitory effect of CH on MDR1 mRNA increased with the concentrations of CH (5.0, 10.0, and 20.0 μM) and the inhibitory effects of CH on MDR1 mRNA and P-glycoprotein increased with the incubation time of CH (0, 12, 24, 36, and 48 hours). The inhibitory effect was weakened after CH combined with SP600125. The expressions of c-Jun and p-c-Jun proteins increased with the incubation time of CH (0, 6, 12, and 24 hours). These findings suggest that CH downregulated the expressions of MDR1 mRNA and P-glycoprotein in a time and concentration manner; the mechanism may be mediated via activating c-Jun/JNK pathway.
Related Links	http://dx.doi.org/10.1155/2014/164391
Starting Page	164391
File Format	PDF
ISSN	23146133
e-ISSN	23146141
Journal	BioMed Research International
Volume Number	2014
Language	English
Publisher	Hindawi Publishing Corporation
Publisher Date	2014-01-01
Access Restriction	Open
Rights Holder	Hindawi Publishing Corporation
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Microbiology Medicine Biochemistry, Genetics and Molecular Biology

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Retracted: Downregulation of MDR1 Gene by Cepharanthine Hydrochloride Is Related to the Activation of c-Jun/JNK in K562/ADR Cells

Retraction Retracted : Downregulation of MDR 1 Gene by Cepharanthine Hydrochloride Is Related to the Activation of c-Jun / JNK in K 562 / ADR Cells

Nerve Injury-Induced c-Jun Activation in Schwann Cells Is JNK Independent

Nerve injury-induced c-Jun activation in Schwann cells is JNK independent.

c-Jun functions as a calcium-regulated transcriptional activator in the absence of JNK/SAPK1 activation.

Arginine methylation of the c-Jun coactivator RACO-1 is required for c-Jun/AP-1 activation

Activation of c-Jun NH2-Terminal Kinase (JNK) Is Required for Gemcitabine’s Cytotoxic Effect in Human Lung Cancer H1299 Cells

Tumor necrosis factor alpha-induced activation of c-jun N-terminal kinase is mediated by TRAF2.

Phosphoacetylation of histone H3 on c-fos- and c-jun-associated nucleosomes upon gene activation

Downregulation of MDR1 Gene by Cepharanthine Hydrochloride Is Related to the Activation of c-Jun/JNK in K562/ADR Cells

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Retracted: Downregulation of MDR1 Gene by Cepharanthine Hydrochloride Is Related to the Activation of c-Jun/JNK in K562/ADR Cells

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Downregulation of MDR1 Gene by Cepharanthine Hydrochloride Is Related to the Activation of c-Jun/JNK in K562/ADR Cells