Two new seco-polycyclic polyprenylated acylphloroglucinol from Hypericum sampsonii

2021 ◽  
Vol 19 (1) ◽  
pp. 216-219
Author(s):  
Zi-Zhen Zhang ◽  
Yan-Rong Zeng ◽  
Ya-Nan Li ◽  
Zhan-Xing Hu ◽  
Lie-Jun Huang ◽  
...  
Keyword(s):  
Multidrug Resistance ◽  
Cancer Cells ◽  
Mdr Reversal ◽  
Mcf 7

Two rare seco-polycyclic polyprenylated acylphloroglucinols (1 and 2) were isolated from Hypericum sampsonii. Compounds 1 and 2 showed moderate multidrug resistance (MDR) reversal activity to resistant cancer cells, HepG2/ADR and MCF-7/ADR.

Design and Syntheses of Permethyl Ningalin B Analogues: Potent Multidrug Resistance (MDR) Reversal Agents of Cancer Cells

2010 ◽  
Vol 53 (14) ◽  
pp. 5108-5120 ◽  
Author(s):  
Pu Yong Zhang ◽  
Iris L. K. Wong ◽  
Clare S. W. Yan ◽  
Xiao Yu Zhang ◽  
Tao Jiang ◽  
...  
Keyword(s):  
Multidrug Resistance ◽  
Cancer Cells ◽  
Reversal Agents ◽  
Mdr Reversal

scholarly journals Induction of multidrug resistance associated protein 2 in tamoxifen-resistant breast cancer cells

2007 ◽  
Vol 14 (2) ◽  
pp. 293-303 ◽  
Author(s):  
Hoo Kyun Choi ◽  
Jin Won Yang ◽  
Sang Hee Roh ◽  
Chang Yeob Han ◽  
Keon Wook Kang
Keyword(s):  
Breast Cancer ◽  
Multidrug Resistance ◽  
Cancer Cells ◽  
Transcriptional Activation ◽  
Breast Cancer Cells ◽  
Pregnane X Receptor ◽  
Pi3 Kinase ◽  
Gene Promoters ◽  
Breast Cancer Patients ◽  
Mcf 7

Acquired resistance to tamoxifen (TAM) is a serious therapeutic problem in breast cancer patients. The transition from chemotherapy-responsive breast cancer cells to chemotherapy-resistant cancer cells is mainly accompanied by the increased expression of multidrug resistance-associated proteins (MRPs). In this study, it was found that TAM-resistant MCF-7 (TAMR-MCF-7) cells expressed higher levels of MRP2 than control MCF-7 cells. Molecular analyses using MRP2 gene promoters supported the involvement of the pregnane X receptor (PXR) in MRP2 overexpression in TAMR-MCF-7 cells. Although CCAAT/enhancer-binding protein β was overexpressed continuously in TAMR-MCF-7 cells, this might not be responsible for the transcriptional activation of the MRP2 gene. In addition, the basal activities of phosphatidylinositol 3-kinase (PI3-kinase) were higher in the TAMR-MCF-7 cells than in the control cells. The inhibition of PI3-kinase significantly reduced both the PXR activity and MRP2 expression in TAMR-MCF-7 cells. Overall, MRP2 induction plays a role in the additional acquisition of chemotherapy resistance in TAM-resistant breast cancer.

scholarly journals JNK1/2 Activation by an Extract from the Roots ofMorus albaL. Reduces the Viability of Multidrug-Resistant MCF-7/Dox Cells by Inhibiting YB-1-Dependent MDR1 Expression

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Youn Kyung Choi ◽  
Sung-Gook Cho ◽  
Hyeong Sim Choi ◽  
Sang-Mi Woo ◽  
Yee Jin Yun ◽  
...  
Keyword(s):  
Gene Expression ◽  
Multidrug Resistance ◽  
Cancer Cells ◽  
Nuclear Translocation ◽  
Multidrug Resistant ◽  
Morus Alba ◽  
Root Extract ◽  
Multidrug Resistance Gene ◽  
Mdr1 Expression ◽  
Mcf 7

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 ofMorus albaL. (White mulberry) reduces doxorubicin-resistant MCF-7/Dox cell viability by inhibiting YB-1 regulation ofMDR1gene expression. When MCF-7 or MCF-7/Dox cells, where MDR1 is highly expressed were treated with an extract from roots or leaves ofMorus albaL., respectively, the root extract from the mulberry (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 ofMDR1gene expression. Moreover, REM promoted phosphorylation of c-Jun NH2-terminal kinase 1/2 (JNK1/2) and JNK1/2 inhibitor, SP600125 and rescued REM inhibition of both MDR1 expression and viabilities in MCF-7/Dox cells. Consistently, overexpression of JNK1, c-Jun, or c-Fos inhibited YB-1-dependent MDR1 expression and reduced viabilities in MCF-7/Dox cells. In conclusion, our data indicate that REM-activated JNK-cJun/c-Fos pathway decreases the viability of MCF-7/Dox cells by inhibiting YB-1-dependentMDR1gene expression. Thus, we suggest that REM may be useful for treating multidrug-resistant cancer cells.

scholarly journals Targeting Cellular Metabolism Chemosensitizes the Doxorubicin-Resistant Human Breast Adenocarcinoma Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Shulan Ma ◽  
Rongfei Jia ◽  
Dongju Li ◽  
Bo Shen
Keyword(s):  
Multidrug Resistance ◽  
Cancer Cells ◽  
Efflux Pump ◽  
Energy Restriction ◽  
Metabolic Energy ◽  
Metabolic Phenotype ◽  
Breast Adenocarcinoma ◽  
Human Breast ◽  
Induced Apoptosis ◽  
Mcf 7

Metabolic energy preferentially produced by glycolysis was an advantageous metabolic phenotype of cancer cells. It is also an essential contributor to the progression of multidrug resistance in cancer cells. By developing human breast cancer MCF-7 cells resistant to doxorubicin (DOX) (MCF-7/MDR cells), the effects and mechanisms of 2-deoxy-D-glucose (2DG), a glucose analogue, on reversing multidrug resistance were investigated. 2DG significantly inhibited the viability of MCF-7/MDR cells and enhanced DOX-induced apoptosis by upregulating protein expression of AMPKα, P53, and caspase-3. The study demonstrated that energy restriction induced by 2DG was relevant to the synergistic effect of 2DG and DOX. The proteins of multidrug gene (the MDR-related protein, MRP1) and P-glycoprotein (P-gp) in MCF-7/MDR cells were downregulated after exposure to 2DG, accompanied with the suppression of the activity of ATP-dependent drug-efflux pump and transmembrane transporter, increasing the intracellular accumulation of DOX to reverse the chemoresistance in multidrug cancer cells.

scholarly journals Development of a Novel Quinoline Derivative as a P-Glycoprotein Inhibitor to Reverse Multidrug Resistance in Cancer Cells

Biology ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 75 ◽  
Author(s):  
Yuanyuan Zhou ◽  
Po-yee Chung ◽  
Jessica Yuen-wuen Ma ◽  
Alfred King-yin Lam ◽  
Simon Law ◽  
...  
Keyword(s):  
Multidrug Resistance ◽  
Cancer Cells ◽  
Cell Lines ◽  
Anticancer Agents ◽  
Underlying Mechanism ◽  
Quinoline Derivative ◽  
Parental Cancer ◽  
Reversal Effect ◽  
P Glycoprotein ◽  
Mdr Reversal

Multidrug resistance (MDR) is one of conventional cancer chemotherapy’s limitations. Our group previously synthesized a series of quinoline-based compounds in an attempt to identify novel anticancer agents. With a molecular docking analysis, the novel compound 160a was predicted to target p-glycoprotein, an MDR candidate. The purpose of this study is to evaluate 160a’s MDR reversal effect and investigate the underlying mechanism at the molecular level. To investigate 160a’s inhibitory effect, we used a series of parental cancer cell lines (A549, LCC6, KYSE150, and MCF-7), the corresponding doxorubicin-resistant cell lines, an MTS cytotoxicity assay, an intracellular doxorubicin accumulation test, and multidrug resistance assays. The Compusyn program confirmed, with a combination index (CI) value greater than 1, that 160a combined with doxorubicin exerts a synergistic effect. Intracellular doxorubicin accumulation and transported calcein acetoxymethyl (AM) (a substrate for p-glycoprotein) were both increased when cancer cells with MDR were treated with compound 160a. We also showed that compound 160a’s MDR reversal effect can persist for at least 1 h. Taken together, these results suggest that the quinoline compound 160a possesses high potential to reverse MDR by inhibiting p-glycoprotein-mediated drug efflux in cancer cells with MDR.

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