ChemInform Abstract: Synthesis of a Novel Series of (E,E)-4,6-Bis(styryl)-2-O-glycopyranosyl-pyrimidines and Their Potent Multidrug Resistance (MDR) Reversal Activity Against Cancer Cells.

ChemInform ◽  
2013 ◽  
Vol 44 (15) ◽  
pp. no-no
Author(s):  
Lei Gao ◽  
Qian Liu ◽  
Sumei Ren ◽  
Shengbiao Wan ◽  
Tao Jiang ◽  
...  
Keyword(s):  
Multidrug Resistance ◽  
Cancer Cells ◽  
Mdr Reversal

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

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.

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.

scholarly journals Dual P-Glycoprotein and CA XII Inhibitors: A New Strategy to Reverse the P-gp Mediated Multidrug Resistance (MDR) in Cancer Cells

Molecules ◽  
2020 ◽  
Vol 25 (7) ◽  
pp. 1748 ◽  
Author(s):  
Elisabetta Teodori ◽  
Laura Braconi ◽  
Silvia Bua ◽  
Andrea Lapucci ◽  
Gianluca Bartolucci ◽  
...  
Keyword(s):  
Multidrug Resistance ◽  
Cancer Cells ◽  
Glycoprotein P ◽  
Reversal Effect ◽  
P Glycoprotein ◽  
New Strategy ◽  
Uptake Test ◽  
New Compounds ◽  
Alkanol Amine ◽  
Mdr Reversal

A new series of N,N-bis(alkanol)amine aryl diesters was synthesized and studied as dual P-glycoprotein (P-gp) and carbonic anhydrase XII inhibitors (CA XII). These hybrids should be able to synergistically overcome P-gp mediated multidrug resistance (MDR) in cancer cells. It was reported that the efflux activity of P-gp could be modulated by CA XII, as the pH reduction caused by CA XII inhibition produces a significant decrease in P-gp ATPase activity. The new compounds reported here feature both P-gp and CA XII binding moieties. These hybrids contain a N,N-bis(alkanol)amine diester scaffold found in P-glycoprotein ligands and a coumarin or benzene sulfonamide moiety to target CA XII. Many compounds displayed a dual activity against P-gp and CA XII being active in the Rhd 123 uptake test on K562/DOX cells and in the hCA XII inhibition test. On LoVo/DOX cells, that overexpress both P-gp and CA XII, some coumarin derivatives showed a high MDR reversal effect in Rhd 123 uptake and doxorubicin cytotoxicity enhancement tests. In particular, compounds 7 and 8 showed higher activity than verapamil and were more potent on LoVo/DOX than on K562/DOX cells overexpressing only P-gp. They can be considered as valuable candidates for selective P-gp/CA XII inhibition in MDR cancer cells.

LDH-doped electrospun short fibers enable dual drug loading and multistage release for chemotherapy of drug-resistant cancer cells

2021 ◽  
Author(s):  
Yupei Ma ◽  
Du Li ◽  
Yunchao Xiao ◽  
Zhijun OuYang ◽  
Mingwu Shen ◽  
...  
Keyword(s):  
Multidrug Resistance ◽  
Cancer Cells ◽  
Cancer Chemotherapy ◽  
Side Effect ◽  
Drug Loading ◽  
Adverse Side Effect ◽  
Drug Resistant ◽  
Short Fibers ◽  
Dual Drug

Conventional cancer chemotherapy is facing difficulties in improving the bioavailability, overcoming the severe adverse side effect of chemotherapeutics and reversing the multidrug resistance of cancer cells. To address these challenges,...

scholarly journals Regulation of Multidrug Resistance in Cancer Cells by Hyaluronan

2003 ◽  
Vol 278 (28) ◽  
pp. 25285-25288 ◽  
Author(s):  
Suniti Misra ◽  
Shibnath Ghatak ◽  
Alexandra Zoltan-Jones ◽  
Bryan P. Toole
Keyword(s):  
Multidrug Resistance ◽  
Cancer Cells

scholarly journals MiR-331-3p Links to Drug Resistance of Pancreatic Cancer Cells by Activating WNT/β-Catenin Signal via ST7L

2020 ◽  
Vol 19 ◽  
pp. 153303382094580
Author(s):  
Ting Zhan ◽  
Xiaoli Chen ◽  
Xia Tian ◽  
Zheng Han ◽  
Meng Liu ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Drug Resistance ◽  
Multidrug Resistance ◽  
Cancer Cells ◽  
Breast Cancer Resistance Protein ◽  
Cancer Resistance ◽  
Multidrug Resistance Protein 1 ◽  
Pancreatic Cancer Cells ◽  
Resistance Protein ◽  
Multidrug Resistance Related Protein

Background: Pancreatic cancer is an aggressive type of cancer with poor prognosis, short survival rate, and high mortality. Drug resistance is a major cause of treatment failure in the disease. MiR-331-3p has been reported to play an important role in several cancers. We previously showed that miR-331-3p is upregulated in pancreatic cancer and promotes pancreatic cancer cell proliferation and epithelial-to-mesenchymal transition–mediated metastasis by targeting ST7L. However, it is uncertain whether miR-331-3p is involved in drug resistance. Methods: We investigated the relationship between miR-331-3p and pancreatic cancer drug resistance. As part of this, microRNA mimics or inhibitors were transfected into pancreatic cancer cells. Quantitative polymerase chain reaction was used to detect miR-331-3p expression, and flow cytometry was used to detect cell apoptosis. The Cell Counting Kit-8 assay was used to measure the IC50 values of gemcitabine in pancreatic cancer cells. The expression of multidrug resistance protein 1, multidrug resistance-related protein 1, breast cancer resistance protein, β-Catenin, c-Myc, Cyclin D1, Bcl-2, and Caspase-3 was evaluated by Western blotting. Results: We confirmed that miR-331-3p is upregulated in gemcitabine-treated pancreatic cancer cells and plasma from chemotherapy patients. We also confirmed that miR-331-3p inhibition decreased drug resistance by regulating cell apoptosis and multidrug resistance protein 1, multidrug resistance-related protein 1, and breast cancer resistance protein expression in pancreatic cancer cells, whereas miR-331-3p overexpression had the opposite effect. We further demonstrated that miR-331-3p effects in drug resistance were partially reversed by ST7L overexpression. In addition, overexpression of miR-331-3p activated Wnt/β-catenin signaling in pancreatic cancer cells, and ST7L overexpression restored activation of Wnt/β-catenin signaling. Conclusions: Taken together, our data demonstrate that miR-331-3p contributes to drug resistance by activating Wnt/β-catenin signaling via ST7L in pancreatic cancer cells. These data provide a theoretical basis for new targeted therapies in the future.

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