Tetrandrine prevents acquired drug resistance of K562 cells through inhibition of mdr1 gene transcription

Shen, Huiling; Xu, Wenlin; Chen, Qiaoyun; Wu, Zhaoyang; Tang, Huarong; Fa-chun, Wang

doi:10.1007/s00432-009-0704-3

Cited by 38 publications

(28 citation statements)

References 14 publications

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“…However, inevitable severe side-effects and multiple drug resistance (MDR) limit its application. The mechanism of chemoresistance is complicated and current research involving reversal of MDR is still in the experimental stage (2)(3)(4). It is necessary to develop novel methods to enhance chemosensitivity and to reverse the MDR.…”

Section: Introductionmentioning

confidence: 99%

Study of the mechanisms underlying the reversal of multidrug resistance of human neuroblastoma multidrug-resistant cell line SK-N-SH/MDR1 by low-intensity pulsed ultrasound

et al. 2013

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Abstract. The aim of the present study was to investigate the underlying mechanism(s) involved in reversing multidrug resistance (MDR) of SK-N-SH/MDR1 by low-intensity pulsed ultrasound (LIPUS). Membrane alteration of SK-N-SH/ MDR1 cells exposed to LIPUS was analyzed by scanning electron microscopy (SEM). Immunofluorescence and western blotting were used\ to detect changes in the expression of the MDR-related proteins P-glycoprotein (P-gp), multidrug resistance protein 1 (MRP1) and glutathione-S-transferase-π (GST-π) after the optimum ultrasonic. The optimum ultrasonic conditions were 0.3 MHz, 1.0 W/cm 2 , 40 sec and the chemosensitivity of SK-N-SH/MDR1 cells was significantly increased (P<0.05). The optimum ultrasonic-induced perforation of the irradiated cell membranes was observed by SEM. The expression of P-gp was significantly decreased in the group treated by optimum ultrasonic (P<0.05), but not the expressions of MRP1 or GST-π (P>0.05). We demonstrated that LIPUS effectively reverses the MDR of SK-N-SH/MDR1, presumably via augmenting membrane permeability and decreasing the P-gp expression of SK-N-SH/MDR1.

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Section: Introductionmentioning

confidence: 99%

Study of the mechanisms underlying the reversal of multidrug resistance of human neuroblastoma multidrug-resistant cell line SK-N-SH/MDR1 by low-intensity pulsed ultrasound

et al. 2013

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“…Therefore, one NF-B binding site is proximal in the human MDR1 gene promoter. Thus, a PCR method can be used with human MDR1 gene primers to ascertain whether NF-B-binding DNA contains the human MDR1 gene and to perform further quantitative comparisons (Shen et al, 2010). In our ChIP-Q-PCR assay, an NF-B p65-specific antibody was used to preferentially precipitate DNA fragments containing the NF-B-binding region present in the regulatory sequences of genes from MCF-7/Adr cells, and the MDR1 gene was chosen as our target gene.…”

Section: Discussionmentioning

confidence: 99%

Key Role of Nuclear Factor-κB in the Cellular Pharmacokinetics of Adriamycin in MCF-7/Adr Cells: The Potential Mechanism for Synergy with 20(S)-Ginsenoside Rh2

Zhang

Meng²,

Zhou³

et al. 2012

Drug Metab Dispos

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ABSTRACT:We have previously demonstrated that ginsenoside 20(S)-Rh2 is a potent ATP-binding cassette (ABC) B1 inhibitor and explored the cellular pharmacokinetic mechanisms for its synergistic effect on the cytotoxicity of Adriamycin. The present studies were conducted to elucidate the key factors that influenced ABCB1 expression, which could further alter Adriamycin cellular pharmacokinetics. Meanwhile, the influence of 20 (

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“…Therefore it's a promising strategy to "prevent" drug-resistance in cancer cells prior to the resistance is formed. Recently, some of the above P-gp down-regulators, such as CsA and tetrandrine, have also been proved the ability to prevent the induction of P-gp expression [11,18] , which is caused by the short-term exposure of native cancer cells to ADM. So in the present study, we turned our research strategy from "reversing" to "preventing" drug resistance in native cancer cells prior to the resistance is formed, and introduced a new member in the class of compounds with activities to prevent the induced drug resistance.…”

Section: Discussionmentioning

confidence: 99%

“…However, it's really hard to reverse when drug resistance is formed because the cancer cells 111111111 have already expressed high level of P-gp and accompanied with many up-stream and down-stream activated targets through cell signaling pathways [8,9] . Therefore, it is promising and important to explore the strategy for preventing or blocking the occurrence of acquired MDR ahead of reversing MDR in the present and future studies [10,11] .…”

Section: Introductionmentioning

confidence: 99%

Curcumin prevents induced drug resistance: A novel function?

Tian

Shen

2011

Chin. J. Cancer Res.

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Objective: We supposed that it will be a promising strategy to "prevent" multidrug resistance (MDR) instead of "reversing" it. This study was designed to investigate the potency of curcumin to prevent the acquired drug resistance induced by adriamycin (ADM) in native K562 cells.Methods: K562 cells were pretreated with curcumin or 0.5% DMSO for 24 h and then were co-incubated with ADM. P-glycoprotein (P-gp) and mdr1 mRNA levels were analyzed separately by flow cytometry and quantitative real-time RT-PCR. The intracellular Rh-123 accumulation was also detected by flow cytometer. Finally, we performed a MTT assay to determine the ADM-induced cytotoxicity with or without pretreatment of curcumin.Results: P-gp and mdr1 mRNA expressions were elevated in the ADM alone group. While in the curcumin pretreated groups, the induced P-gp and mdr1 mRNA levels gradually decreased with increasing curcumin concentrations, and the Rh-123 accumulation level was almost recovered close to the control group's. Finally, the MTT colorimetric assay verified the enhanced effect of curcumin on ADM-induced cytotoxicity.Conclusion: Our present study suggested that curcumin exhibits the novel ability to prevent the up-regulation of P-gp and its mRNA induced by ADM. The prevention capacity is also functionally associated with the elevated intracellular drug accumulation and parallel enhanced ADM cytotoxicity. We revealed a novel function of curcumin as a potential drug resistance preventor.

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Tetrandrine prevents acquired drug resistance of K562 cells through inhibition of mdr1 gene transcription

Abstract: In summary, tetrandrine can prevent doxorubicin-induced mdr1 mRNA/P-gp expression and P-gp functions in a dose-dependent manner through a mechanism that may involve inhibition of doxorubicin-induced NF-kappaB mRNA expression and protein activity.

Cited by 38 publications

References 14 publications

Study of the mechanisms underlying the reversal of multidrug resistance of human neuroblastoma multidrug-resistant cell line SK-N-SH/MDR1 by low-intensity pulsed ultrasound

Study of the mechanisms underlying the reversal of multidrug resistance of human neuroblastoma multidrug-resistant cell line SK-N-SH/MDR1 by low-intensity pulsed ultrasound

Key Role of Nuclear Factor-κB in the Cellular Pharmacokinetics of Adriamycin in MCF-7/Adr Cells: The Potential Mechanism for Synergy with 20(S)-Ginsenoside Rh2

Curcumin prevents induced drug resistance: A novel function?

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