6 results on '"Zhao, Yongfu"'
Search Results
2. Low density lipoprotein receptor (LDLR)-targeted lipid nanoparticles for the delivery of sorafenib and Dihydroartemisinin in liver cancers.
- Author
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Wang Z, Duan X, Lv Y, and Zhao Y
- Subjects
- Animals, Antineoplastic Agents administration & dosage, Antineoplastic Agents, Phytogenic administration & dosage, Antineoplastic Combined Chemotherapy Protocols pharmacokinetics, Artemisinins administration & dosage, Cell Survival drug effects, Drug Delivery Systems, Hep G2 Cells, Humans, Mice, Mice, Inbred BALB C, Neoplasm Transplantation, Reactive Oxygen Species metabolism, Sorafenib administration & dosage, Antineoplastic Combined Chemotherapy Protocols administration & dosage, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Lipids pharmacology, Liver Neoplasms drug therapy, Nanoparticles, Receptors, LDL drug effects
- Abstract
Aims: Liver cancer is one of the leading causes of cancer mortality worldwide. Inspired by the biological structure and function of low-density lipoprotein (LDL), in this study, an ApopB-100 based targeted lipid nanoparticles was synthesized to improve the therapeutic efficacy in liver cancer treatment., Main Methods: The biological composition of ApopB is similar to LDL which can effectively increase the targeting efficiency of nanoparticles in LDL receptor (LDLR)-overexpressed liver tumors., Keyfindings: We have demonstrated that the co-administration of sorafenib (SRF) and Dihydroartemisinin (DHA) could exhibit synergistic anticancer effect in HepG2 liver cancer cells. DHA produced excessive cellular reactive oxygen species (ROS) and induced greater apoptosis of cancer cells. LDL-based SRF/DHA-loaded lipid nanoparticles (LD-SDN) showed remarkable decrease in the cell viability compared to that of either of single drug treated cancer cells. Combination of SRF+DHA resulted in predominant SubG1 proportion of cells. LD-SDN exhibited the highest SubG1 (%) of cells compared to that of any of the individual drugs. Most importantly, robust antitumor response and delayed tumor growth was observed for LD-SDN treated xenograft tumor model. Ki67 proliferation index of LD-SDN (22.1 ± 5.6%) is significantly lesser compared to that of either control (86.2 ± 6.9%) or SRF (75.4 ± 4.89%) or DHA (69.4 ± 6.9%)., Significances: These data provide strong evidence that LDL-mimetic lipid nanoformulations could be utilized as a biocompatible and tumor targeted platform for the delivery of multiple anticancer drugs in cancer treatment., (Copyright © 2019 Elsevier Inc. All rights reserved.)
- Published
- 2019
- Full Text
- View/download PDF
3. Aspirin overcomes Navitoclax-resistance in hepatocellular carcinoma cells through suppression of Mcl-1.
- Author
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Li G, Zhang S, Fang H, Yan B, Zhao Y, Feng L, Ma X, and Ye X
- Subjects
- Anti-Inflammatory Agents, Non-Steroidal pharmacology, Antineoplastic Agents pharmacology, Apoptosis drug effects, Blotting, Western, Carcinoma, Hepatocellular genetics, Carcinoma, Hepatocellular metabolism, Carcinoma, Hepatocellular pathology, Caspase 3 metabolism, Caspase 9 metabolism, Cell Line, Tumor, Cell Survival drug effects, Cysteine Proteinase Inhibitors pharmacology, Cytochromes c metabolism, Dose-Response Relationship, Drug, Drug Synergism, Hep G2 Cells, Humans, Liver Neoplasms genetics, Liver Neoplasms metabolism, Liver Neoplasms pathology, Myeloid Cell Leukemia Sequence 1 Protein, Oligopeptides pharmacology, Proto-Oncogene Proteins c-bcl-2 genetics, RNA Interference, Aniline Compounds pharmacology, Aspirin pharmacology, Drug Resistance, Neoplasm drug effects, Proto-Oncogene Proteins c-bcl-2 metabolism, Sulfonamides pharmacology
- Abstract
Small-molecule Bcl-2/Bcl-xL inhibitor Navitoclax represents a promising cancer therapeutic since preclinical and clinical studies with Navitoclax have demonstrated strong anticancer activity in several types of cancers. However, because Navitoclax has a low binding affinity to Mcl-1, anticancer activity by Navitoclax is often attenuated by the elevated expression of Mcl-1 in hepatocellular carcinoma (HCC) and other cancers, posing a serious problem for its potential clinical utilities. Therefore, approaches that suppress the expression of Mcl-1 are urgently needed to overcome Navitoclax-resistance in these cancers. Here, we reported that aspirin markedly suppressed Mcl-1 expression, and significantly enhanced Navitoclax-mediated cell viability inhibition and apoptosis induction in HCC cells. We further showed that aspirin robustly enhanced Navitoclax-triggered cytosolic cytochrome c release, activation of initiator caspase-9 and effector caspase-3, and cleavage of PARP. Importantly, the cell death induction by the combination could be rescued by a cell-permeable caspase-9 inhibitor Z-LEHD-FMK, indicative of an indispensable role of mitochondrial apoptosis pathway during the combination effect. Taken together, our study suggests that aspirin can be used to enhance Navitoclax-mediated anticancer activity via suppression of Mcl-1. Since aspirin is one of the most commonly used medicines, our findings therefore have translational impacts on Navitoclax-based therapy for HCC., (Copyright © 2013 Elsevier Inc. All rights reserved.)
- Published
- 2013
- Full Text
- View/download PDF
4. Glycogenes mediate the invasive properties and chemosensitivity of human hepatocarcinoma cells.
- Author
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Guo R, Cheng L, Zhao Y, Zhang J, Liu C, Zhou H, and Jia L
- Subjects
- Animals, Antimetabolites, Antineoplastic pharmacology, Carcinoma, Hepatocellular drug therapy, Carcinoma, Hepatocellular pathology, Cell Line, Tumor, Fluorouracil pharmacology, Gene Expression, Glycosylation, Glycosyltransferases metabolism, Humans, Lectins metabolism, Liver Neoplasms, Experimental drug therapy, Liver Neoplasms, Experimental pathology, Male, Mice, Mice, Nude, Neoplasm Invasiveness, Oligonucleotide Array Sequence Analysis, Protein Binding, Protein Processing, Post-Translational, Transcriptome, Tumor Burden drug effects, Xenograft Model Antitumor Assays, Carcinoma, Hepatocellular enzymology, Cell Movement, Drug Resistance, Neoplasm, Glycosyltransferases genetics, Liver Neoplasms, Experimental enzymology
- Abstract
Aberrant cell-surface glycosylation patterns are present on tumors and have been linked to tumor progression. This study aimed to identify the alterations of glycogene and N-glycan involved in tumor invasion, tumorigenicity and drug resistance in MHCC97-H and MHCC97-L human hepatocarcinoma cell lines, which have high, low metastatic potential, respectively. Using real-time PCR for quantification of glycogene and FITC-lectin binding for glycan profiling, we found that the expression of glycogenes and glycan profiling were different in MHCC97-H cells, as compared to those in MHCC97-L cells. We silenced the expression levels of glycogenes MGAT3 and MGAT5, which were over-expressed in MHCC97-L and MHCC97-H cells. Knockdown of MGAT3 expression promoted MHCC97-L cells invasion and increased resistance to 5-fluorouracil in vitro. The silencing of MGAT5 in MHCC97-H cells inhibited invasion and increased sensitivity to 5-fluorouracil in vitro. Further analysis of the N-glycan regulation by tunicamycin application or PNGase F treatment in MHCC97-H and MHCC97-L cells showed partial inhibition of N-glycan glycosylation, decreased invasion, tumorigenicity and increased sensitivity to 5-fluorouracil both in vitro and in vivo. These findings suggest that alterations of glycogene and N-glycan in human hepatocarcinoma cells correlate with tumor invasion, tumorigenicity and sensitivity to chemotherapeutic drug, and have significant implications for the development of treatment strategies., (Copyright © 2012 Elsevier Ltd. All rights reserved.)
- Published
- 2013
- Full Text
- View/download PDF
5. Glycomic alterations are associated with multidrug resistance in human leukemia.
- Author
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Zhang Z, Zhao Y, Jiang L, Miao X, Zhou H, and Jia L
- Subjects
- Antineoplastic Agents pharmacology, Blotting, Western, Cell Survival drug effects, Doxorubicin pharmacology, Flow Cytometry, Fluorescein-5-isothiocyanate metabolism, Gene Expression Regulation, Neoplastic, Humans, K562 Cells, Lectins metabolism, Leukemia genetics, Leukemia metabolism, Leukemia pathology, N-Acetylglucosaminyltransferases genetics, N-Acetylglucosaminyltransferases metabolism, Paclitaxel pharmacology, Peptide-N4-(N-acetyl-beta-glucosaminyl) Asparagine Amidase metabolism, Polysaccharides metabolism, Protein Binding, RNA Interference, Reverse Transcriptase Polymerase Chain Reaction, Sialyltransferases genetics, Sialyltransferases metabolism, Tunicamycin pharmacology, Vincristine pharmacology, Drug Resistance, Multiple, Drug Resistance, Neoplasm, Glycomics methods, Polysaccharides biosynthesis
- Abstract
Correlations of disease phenotypes with glycosylation changes have been analyzed intensively in tumor biology field. In this study we describe glycomic alterations of multidrug resistance in human leukemia cell lines. Using multiple glycan profiling tools: real-time PCR for quantification of glycogenes, FITC-lectin binding for glycan profiling, and mass spectrometry for glycan composition, we compared the glycomics of drug-resistant K562/ADR cells with parental K562 line. The results showed that the expression of glycogenes, glycan profiling and N-glycan composition were different in K562/ADR cells, as compared with those in K562 cells, whereas O-glycans of the two cell lines showed no different mass spectra. Further analysis of the N-glycan regulation by way of tunicamycin application or PNGase F treatment in K562/ADR cells showed partial inhibition of biosynthesis and increased sensitivity to chemotherapeutic drugs in vitro. We targeted glycogene B3GNT8 and ST8SIA4, which were over-expressed in K562/ADR cells, and silenced the expression levels of two glycogenes after using RNA interference approach. The results showed that the silencing of B3GNT8 or ST8SIA4 in K562/ADR cells resulted in increased chemosensitivity to anti-tumor drugs. In conclusion, glycomic alterations are responsible for the overcoming multidrug resistance in human leukemia therapy and the N-linked oligosaccharides are associated with the drug resistance of cancer cells., (Copyright © 2012 Elsevier Ltd. All rights reserved.)
- Published
- 2012
- Full Text
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6. Radiation-induced reduction of diuron by gamma-ray irradiation.
- Author
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Zhang J, Zheng Z, Zhao T, Zhao Y, Wang L, Zhong Y, and Xu Y
- Subjects
- Carbon chemistry, Chlorine analysis, Chlorine chemistry, Dose-Response Relationship, Radiation, Gamma Rays, Hazardous Substances analysis, Hydrochloric Acid chemistry, Hydrogen-Ion Concentration, Ions, Kinetics, Models, Chemical, Sodium Hydroxide chemistry, Time Factors, Ultraviolet Rays, Water Purification methods, Diuron chemistry
- Abstract
Diuron degradation efficiencies and the proposed mechanism by gamma-ray irradiation were investigated. Several factors that might affect the degradation values were further examined. The UV absorbances at 200-400 nm and diuron concentration decreased with the increase of radiation dose. When diuron initial concentration was 18.5 mg L(-1) and 1.0 kGy was selected as the radiation dose, diuron removal value and loss of total organic carbon were 100 and 34.1%, respectively. However, the concentration of Cl- ion increased with the increase of radiation dose. The process could be depicted by first order reaction kinetics and the reaction was mainly caused by the reaction of diuron with .OH and eaq-. The degradation efficiency decreased with the increase of initial concentration at the same radiation dose. H2O2, HCO3-, NO3-, NO2-, CH3OH and humic acid as additives reduced the degradation efficiency. Furthermore, the increase of NO3-, NO2-, CH3OH and humic acid would result in the decrease of the degradation values. The pH value could affect the removal efficiency and the degradation process was enhanced in acid condition. The pH value became lower with increasing radiation dose after gamma-ray irradiation.
- Published
- 2008
- Full Text
- View/download PDF
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