5 results on '"Xu, Xiao-fang"'
Search Results
2. Synthesis, structural characterization and antitumor activity of six rare earth metal complexes with 8-hydroxyquinoline derivatives.
- Author
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Yang QY, Cao QQ, Zhang YL, Xu XF, Deng CX, Kumar R, Zhu XM, Wang XJ, Liang H, and Chen ZF
- Subjects
- Antineoplastic Agents chemistry, Apoptosis drug effects, Cell Cycle drug effects, Cell Line, Tumor, Cisplatin pharmacology, Coordination Complexes chemistry, Humans, Metals, Rare Earth chemistry, Neoplasms chemistry, Neoplasms metabolism, Oxyquinoline pharmacology, Signal Transduction drug effects, Antineoplastic Agents pharmacology, Coordination Complexes pharmacology, Metals, Rare Earth pharmacology, Mitochondria drug effects, Neoplasms drug therapy, Oxyquinoline chemistry
- Abstract
The rare earth metal Gd(III), Yb(III), Lu(III), Eu(III), Tb(III) and Ho(III) complexes 1-6 with 2-((2-(pyridin-2-yl)hydrazono)methyl)quinolin-8-ol (H-L) as ligands were synthesized. The in vitro cytotoxicity assay indicated that the cytotoxicity of 1 was equivalent to cisplatin and higher than that of H-L and other complexes towards T24 tumor cells. The mechanism study indicated that 1 caused significant up-regulation of the proteins p27, p21 and p53 in T24 cells and cell cycle arrest in G2 phase. In addition, 1 induced effective T24 cells apoptosis via mitochondrial dysfunction pathway, which was indicated by changes in mitochondrial membrane potential (Δψ), reactive oxygen species (ROS), intracellular Ca
2+ and the mitochondria-related proteins (including cytochrome C (Cyt C), B-cell lymphoma-2 (Bcl-2), Bcl-2-associated x (Bax) and apoptotic protease activating factor-1 (Apaf-1)). Moreover, 1 could activate caspase-3/8/9 in T24 cells. Therefore, complex 1 is a promising and potent anticancer drug candidate., Competing Interests: Declaration of competing interest All authors declare no conflict of interest for this work., (Copyright © 2020 Elsevier Inc. All rights reserved.)- Published
- 2020
- Full Text
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3. Novel virosecurinine bivalent mimetics as potent reversal agents against P-glycoprotein-mediated multidrug resistance.
- Author
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Hou W, Meng Y, Xu XF, Huang ZX, Liu J, Wang ZY, Lin J, and Chen WM
- Subjects
- Animals, Cell Line, Tumor, Cell Survival drug effects, Doxorubicin pharmacology, Heterocyclic Compounds, Bridged-Ring chemistry, Heterocyclic Compounds, Bridged-Ring pharmacology, Humans, Male, Mice, Inbred BALB C, Mice, Nude, Verapamil pharmacology, ATP Binding Cassette Transporter, Subfamily B, Member 1 antagonists & inhibitors, Alkaloids chemistry, Alkaloids pharmacology, Antineoplastic Agents chemistry, Antineoplastic Agents pharmacology, Azepines chemistry, Azepines pharmacology, Drug Resistance, Multiple drug effects, Drug Resistance, Neoplasm drug effects, Lactones chemistry, Lactones pharmacology, Piperidines chemistry, Piperidines pharmacology
- Abstract
Multidrug resistance (MDR) is a main cause of chemotherapy failure and patient death. This situation usually involves a glycoprotein (P-gp) mediated drug efflux, resulting in a low cellular drug concentration and insensitivity. Here we report the design, synthesis and evaluation of novel (+/-)-securinine bivalents as P-gp inhibitors in vitro and in vivo. MTT assays reflected that bivalent mimetics of securinine particularly the virosecurinine bivalent mimetic 8C showed promissing MDR reversal potential in both P-gp highly expressed cell line HepG2/DOX and MCF-7/ADM. At a 10 μM concentration, 8C can entirely reverse the resistance of HepG2/DOX to doxorubicin (DOX), and is more effective than the positive control verapamil (VRP). Fluorescence, flow cytometry, and DOX efflux assays demonstrated that 8C can facilitate the accumulation and diminish the efflux of intracellular DOX. Molecular docking analysis and western blot assays indicated that 8C accomplished this by competitively inhibiting the activity of P-gp rather than by affecting its expression. Compound 8C was also observed to reverse drug resistance effectively in xenograft models when combined with DOX. This study lays a foundation for the discovery of (+/-)-securinine ramifications as P-gp inhibitors and provides a promising lead compound 8C as a P-gp mediated MDR reversal agent., (Copyright © 2019 Elsevier Masson SAS. All rights reserved.)
- Published
- 2019
- Full Text
- View/download PDF
4. Nuclear translocation of MRP1 contributes to multidrug resistance of mucoepidermoid carcinoma.
- Author
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Cai BL, Xu XF, Fu SM, Shen LL, Zhang J, Guan SM, and Wu JZ
- Subjects
- ATP Binding Cassette Transporter, Subfamily B, Member 1 genetics, ATP Binding Cassette Transporter, Subfamily B, Member 1 metabolism, Antibiotics, Antineoplastic pharmacology, Antimetabolites, Antineoplastic pharmacology, Bleomycin analogs & derivatives, Bleomycin pharmacology, Blotting, Western, Carcinoma, Mucoepidermoid metabolism, Cell Line, Tumor, Cisplatin pharmacology, Doxorubicin pharmacology, Epirubicin pharmacology, Fluorescent Antibody Technique, Indirect, Fluorouracil pharmacology, Humans, Paclitaxel pharmacology, Reverse Transcriptase Polymerase Chain Reaction, Salivary Gland Neoplasms metabolism, ATP Binding Cassette Transporter, Subfamily B, Member 1 drug effects, Antineoplastic Agents pharmacology, Carcinoma, Mucoepidermoid genetics, Drug Resistance, Multiple genetics, Drug Resistance, Neoplasm genetics, Salivary Gland Neoplasms genetics
- Abstract
Multidrug resistance-related protein 1 (MRP1 or ABCC1), a membrane-bound energy-dependent efflux transporter, is overexpressed in several kinds of multidrug-resistant cell lines and related to multidrug-resistance (MDR) of various cancers. In this study, we investigated whether MRP1 was involved in the chemoresistance of mucoepidermoid carcinoma (MEC). We demonstrated that down-regulation of MRP1 in MC3/5FU, a drug-resistant MEC cell line, by RNA interference increased the drug sensitivity of the cells to 5-fluorouracil, doxorubicin, pharmorubicin, bleomycin-A5, cis-platinum and taxol. However, no significant quantitative difference of MRP1 mRNA and protein expression was found between MC3/5FU cells and its parental cell line (MC3) as determined by RT-PCR and Western blot. Interestingly, MRP1 was translocated from the cytoplasmic membrane of the MC3 cells to the nuclei of MC3/5FU cells as revealed by indirect immunofluorescence staining. Furthermore, MRP1 down-regulation mainly decreased the nuclear expression of MRP1 rather than the cytoplasmic membrane expression. Our results suggested that MRP1 was involved in the chemoresistance of MEC and MRP1 may confer drug-resistance by a mechanism associated with its nuclear translocation., (Copyright © 2011 Elsevier Ltd. All rights reserved.)
- Published
- 2011
- Full Text
- View/download PDF
5. Arene‐Ruthenium(II)/Osmium(II) Complexes Potentiate the Anticancer Efficacy of Metformin via Glucose Metabolism Reprogramming.
- Author
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Yang, Qi‐Yuan, Ma, Rui, Gu, Yun‐Qiong, Xu, Xiao‐Fang, Chen, Zhen‐Feng, and Liang, Hong
- Subjects
GLUCOSE metabolism ,ANTINEOPLASTIC agents ,BLOOD sugar ,LIVER metastasis ,METFORMIN ,METASTASIS - Abstract
Targeting metabolic reprogramming to treat cancer could increase overall survival and reduce side effects. Here, we put forward a strategy using arene‐ruthenium(II)/osmium(II) complexes to potentiate the anticancer effect of metformin (Met.) via glucose metabolism reprogramming. Complexes 1–6 with oxoglaucine derivatives as ligands were synthesized and their anti‐tumor activities were tested under hypoglycemia. Results indicated that 2 and 5 potentiated the anticancer effects of Met. under hypoglycemia, exhibiting lower toxicity, slower blood glucose decline and inhibition of early tumor liver metastasis. Combination of 5 with Met. could be used as a new strategy to treat cancer under hypoglycemia through glucose metabolism reprogramming. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
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