Radiosensitivity of hepatoma cell lines and human normal liver cell lines exposed in vitro to carbon ions and argon ions at the HIRFL

2009 ◽  
Vol 267 (10) ◽  
pp. 1837-1840 ◽  
Author(s):  
Xigang Jing ◽  
Wenjian Li ◽  
Zhuanzi Wang ◽  
Wei Wei ◽  
Chuanling Guo ◽  
...  
Keyword(s):  
Cell Lines ◽  
Liver Cell ◽  
Hepatoma Cell ◽  
Normal Liver ◽  
Carbon Ions ◽  
Normal Liver Cell ◽  
Hepatoma Cell Lines ◽  
Argon Ions

scholarly journals Heparin and Liver Heparan Sulfate Can Rescue Hepatoma Cells from Topotecan Action

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
József Dudás ◽  
József Bocsi ◽  
Alexandra Fullár ◽  
Kornélia Baghy ◽  
Tibor Füle ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Heparan Sulfate ◽  
Cell Lines ◽  
Topoisomerase I ◽  
Hepatoma Cell ◽  
Normal Liver ◽  
Hepatoma Cell Lines ◽  
Inhibitory Compound ◽  
Hep3b Cells

Topotecan (TpT) is a major inhibitory compound of topoisomerase (topo) I that plays important roles in gene transcription and cell division. We have previously reported that heparin and heparan sulfate (HS) might be transported to the cell nucleus and they can interact with topoisomerase I. We hypothesized that heparin and HS might interfere with the action of TpT. To test this hypothesis we isolated topoisomerase I containing cell nuclear protein fractions from normal liver, liver cancer tissues, and hepatoma cell lines. The enzymatic activity of these extracts was measured in the presence of heparin, liver HS, and liver cancer HS. In addition, topo I activity, cell viability, and apoptosis of HepG2 and Hep3B cells were investigated after heparin and TpT treatments. Liver cancer HS inhibited topo I activity in vitro. Heparin treatment abrogated topo I enzyme activity in Hep3B cells, but not in HepG2 cells, where the basal activity was higher. Heparin protected the two hepatoma cell lines from TpT actions and decreased the rate of TpT induced S phase block and cell death. These results suggest that heparin and HS might interfere with the function of TpT in liver and liver cancer.

scholarly journals Design, Syntheses and Antitumor Activities Evaluation of 1,5-diaryl Substituted Pyrazole Secnidazole Ester Derivatives

2021 ◽  
Author(s):  
Qing-Hu Teng ◽  
Gui-Xia Sun ◽  
Shu-Ying Luo ◽  
kai wang ◽  
Fu-Pei Liang
Keyword(s):  
Tumor Cell ◽  
Cell Lines ◽  
Liver Cell ◽  
Lung Tumor ◽  
Normal Liver ◽  
Inhibition Mechanism ◽  
Normal Liver Cell ◽  
Human Liver Cell ◽  
Induced Apoptosis

Abstract According to the drug hybridization principle, a series of novel 1,5-diaryl substituted pyrazole secnidazole ester derivatives (6aa-6gc) have been synthesized by the combinations of various 1,5-diarylpyrazole-3-carboxylic acids with secnidazole. The in vitro antitumor/cytotoxicities activities against tumor and normal cell lines, including NCI-H460 (lung tumor cell), MCG-803 (gastric tumor cell), Skov-3 (ovarian tumor cell), BEL-7404 (liver tumor cell) and HL-7702 (normal liver cell), have been evaluated using MTT assay. All compounds showed promising inhibitory activities against four tumor cell lines. The IC50 of 6bc against the BEL-7404 cell was 2.03 μM, and those of 6fc against the NCI-H460, MCG-803 and Skov-3 were 1.34, 0.14 and 0.87 μM, respectively. All these values were much lower than those of the cisplatin. Furthermore, 6fc and 6bc were also verified to be considerable safe for normal human liver cell, since the lower IC50 values than cisplatin. Based on these results, the cell cycle analysis, apoptosis ratio detection, and mitochondrial membrane potential assay of 6fc and 6bc were further performed aiming to investigate their inhibition mechanism of BEL-7404 cells. It is revealed that they have effectively inhibited the cell growth by arresting the BEL-7404 cells at S phase and induced apoptosis through the mitochondria-mediated pathway.

Different Expression of Esterase Variants in Rat Hepatic and Hepatom a-Derived Cell Lines Detected by Electrophoresis

1995 ◽  
Vol 50 (9-10) ◽  
pp. 664-668 ◽  
Author(s):  
Adel S. Afify ◽  
Yoshimitsu Yamazaki ◽  
Yu-ichi Kageyama ◽  
Shiro Yusa ◽  
Yoshikatsu Ogawa ◽  
...  
Keyword(s):  
Cell Lines ◽  
Rat Liver ◽  
Hepatoma Cell ◽  
Polyacrylamide Gel Electrophoresis ◽  
Liver Homogenate ◽  
Normal Liver ◽  
Liver Parenchyma ◽  
Hepatoma Cell Lines ◽  
Normal Rat ◽  
Transformed Cell Lines

Abstract Esterases in nine rat hepatic and hepatoma-derived cell lines and normal rat liver homogenate were detected by polyacrylamide gel electrophoresis coupled with active staining with a-naphthyl acetate or butyrate as a substrate. The esterase band patterns of the non-cancerous and oncogene-transformed cell lines were alike, but different from those of hepatoma cell lines and normal rat liver homogenate. The former groups of cells might have completely lost the characteristics of rat liver parenchymal cells, or else they might have their origin at cells other than liver parenchyma. The esterase patterns of the hepatoma cell lines (e.g., McA-RH7777) and the normal rat liver highly resembled with each other, exemplifying the slight biochemical deviation of cancer from normal cells. However, two-dimensional electrophoretogram for the McA-RH7777 cell line showed a prominent esterase spot {p/ 6.0-Mr 110 kDa) that was lacking in the normal liver. This result indicates that there is invariably some change in esterase expression between the cancer cells and the normal liver cells

Looking for synergy or additivity between 188Re and sorafenib on hepatoma cell lines.

2012 ◽  
Vol 30 (4_suppl) ◽  
pp. 247-247
Author(s):  
Marc Pracht ◽  
Nicolas Lepareur ◽  
Julien Edeline ◽  
Laurence Lenoir ◽  
Valerie Ardisson ◽  
...  
Keyword(s):  
Cell Line ◽  
Hepg2 Cell ◽  
Cell Lines ◽  
Hepatoma Cell ◽  
External Beam Radiotherapy ◽  
Combined Treatment ◽  
Hepatoma Cell Lines ◽  
Heparg Cell Line

247 Background: In case of non resectable HCC, radioembolization and sorafenib (S) are therapeutic options respectively for intermediate and advanced stages. In some other cancers, there is an increase of efficacy when external beam radiotherapy is done concomitantly with systemic chemotherapy or targeted therapies. So we wondered if there could be a synergistic or an additive activity when S is combined with a radionuclide. Methods: Hepatoma cell lines N1S1 (murine HCC), HepG2 (human hepatoblastoma) and HepaRG (human HCC) were treated with increasing concentrations of rhenium-188 (188Re) or S. On each cell line, we have studied the cellular toxicities of S and 188Re using Tetrazolium dye test, extra-cellular medium LDH level and morphologic analysis. This was done for different dosage of S and 188Re. We measured the lethal concentration killing 25% of cells (LC25) with the results of the Tetrazolium dye test. Secondly, we looked for synergy or additivity on cellular toxicity of these two compounds according to cell lines by combined treatment. Synergy or additivity was estimated with the combination index (CI) method (synergy if CI lower than 1, additivity if CI = 1, antagonism if CI upper to 1) based on the Tetrazolium dye test’s results. Results: Monotherapy dose-dependent toxicities were observed for all three cell lines with 188Re and for the N1S1 and HepG2 cell lines only with S. Combined treatment with 188Re and S showed synergy on HepaRG and N1S1 cell lines and additivity on the HepG2 cell line. Conclusions: The additive, and even synergistic, interest of a combined treatment with 188Re and S is demonstrated in vitro (for the first time to our knowledge) on hepatoma cell lines. This results, in particular for the HepaRG cell line (human HCC), could be explained by the down-regulation of the hepatic drug transporters which are responsible for the Sorafenib efflux in case of simultaneous DNA damages due to a radionuclide exposition. This promising approach now needs to be confirmed in vivo. [Table: see text]

scholarly journals AS-30D hepatoma as a model to study on insulin resistance in vitro.

2013 ◽  
Vol 60 (4) ◽  
Author(s):  
Katarzyna Wierzbicka-Bregier ◽  
Wojciech Brutkowski ◽  
Anna Borkowska ◽  
Krzysztof Milewski ◽  
Krzysztof Zabłocki
Keyword(s):  
Insulin Resistance ◽  
Cell Lines ◽  
Hepatoma Cell ◽  
Cellular Level ◽  
Ros Generation ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Hepatoma Cell Lines ◽  
Kinase Phosphorylation

Studies on insulin resistance of liver cells are often performed with the use of various hepatoma cell lines. Such an approach allows investigating selected biochemical pathways at the cellular level. However, possible modifications of metabolic processes due to the neoplastic nature of such cells must be considered. Expanding the diversity of hepatoma cell lines used in metabolic studies could deliver new data for comparison with those obtained for other cell lines and should reduce the risk of misleading conclusions. In this study rat hepatoma AS-30D cells were tested as a potential model for studies on palmitate-induced insulin resistance. It was found that insulin-induced Akt kinase phosphorylation was substantially reduced in cells incubated with palmitate at a concentration as low as 75 µM. This effect was not accompanied by excessive reactive oxygen species (ROS) generation or increased Jun N-terminal kinase (JNK) phosphorylation. Moreover, preincubation of AS-30D cells with rosiglitazone, an antidiabetic agonist of peroxisome proliferator-activated receptor gamma (PPARγ), efficiently prevented the palmitate-induced insulin resistance. We conclude that AS-30D hepatoma cells may be used as a model sensitive to insulin and vulnerable to palmitate-induced insulin resistance.

Sign in / Sign up

Export Citation Format

Share Document