Abstract No. 270: Differential effect of therapeutic hyperthermia on cellular viability, death and survival in an in vitro model of hepatocellular carcinoma

2012 ◽  
Vol 23 (3) ◽  
pp. S110
Author(s):  
S.M. Thompson ◽  
M.R. Callstrom ◽  
K.A. Butters ◽  
J.P. Grande ◽  
L.R. Roberts ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Differential Effect ◽  
In Vitro Model ◽  
Cellular Viability ◽  
Therapeutic Hyperthermia ◽  
Vitro Model

Assessment of supra-additive effects of cytotoxic drugs and low dose rate irradiation in an in vitro model for hepatocellular carcinoma

2006 ◽  
Vol 84 (10) ◽  
pp. 1021-1028 ◽  
Author(s):  
Bieke Lambert ◽  
Leo De Ridder ◽  
Filip De Vos ◽  
Guido Slegers ◽  
Virginie de Gelder ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Dose Rate ◽  
In Vitro Model ◽  
Low Dose ◽  
High Dose ◽  
Additive Effects ◽  
Multicellular Spheroids ◽  
Low Dose Rate ◽  
Vitro Model

The use of 5-fluorouracil, topotecan, or gemcitabine was tested for enhancement of the effects of low dose rate (LDR) irradiation in an in vitro model for hepatocellular carcinoma. For comparison, all drugs were tested in combination with high dose rate (HDR) γ-irradiation as well. Multicellular spheroids of HepG2 cells were exposed to HDR or LDR irradiation by means of external beam cobalt-60 or rhenium-188 (188Re), respectively, dissolved in the culture medium. Secondly, exposure to irradiation was combined with the cytotoxic drug. Toxicity was evaluated by means of a quantitative spheroid outgrowth assay and histology. For 5-fluorouracil, supra-additive effects were observed in combination with HDR irradiation. With 188Re, the supra-additive toxicity was only transient. For topotecan and 188Re, no supra-additive effects were seen, whereas the addition of HDR irradiation at the end of the topotecan exposure yielded lasting supra-additive effects. Incubation with gemcitabine followed by exposure to HDR irradiation, induced a synergistic toxicity on the outgrowth. No supra-additive effects were observed when HDR irradiation was added at the start of the incubation with gemcitabine or combined with LDR irradiation. For all drugs tested, supra-additive effects were observed with HDR irradiation if the timing of the irradiation was appropriate. For 188Re, no lasting supra-additive effects were observed.

scholarly journals Silibinin inhibits ethanol metabolism and ethanol-dependent cell proliferation in an in vitro model of hepatocellular carcinoma

2010 ◽  
Vol 291 (1) ◽  
pp. 120-129 ◽  
Author(s):  
Elizabeth Brandon-Warner ◽  
James A. Sugg ◽  
Laura W. Schrum ◽  
Iain H. McKillop
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
In Vitro Model ◽  
Ethanol Metabolism ◽  
Dependent Cell ◽  
Vitro Model

Screening for supra-additive effects of cytotoxic drugs and gamma irradiation in an in vitro model for hepatocellular carcinoma

2004 ◽  
Vol 82 (2) ◽  
pp. 146-152 ◽  
Author(s):  
B Lambert ◽  
L De Ridder ◽  
G Slegers ◽  
V de Gelder ◽  
R A Dierckx ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Gamma Irradiation ◽  
In Vitro Model ◽  
Palliative Therapy ◽  
Cytotoxic Drugs ◽  
Treatment Modalities ◽  
Additive Effects ◽  
Vitro Model

Hepatocellular carcinoma (HCC) is one of the most common malignancies in the world. A wide variety of treatment modalities is available for palliative therapy of HCC, although there is no strong evidence that these treatments can have a significant impact on survival. The aim of this work was to screen cytotoxic drugs relevant in the treatment of HCC for enhancement of the effect of irradiation in an in vitro model. As the majority of patients presenting with HCC suffer reduced liver function, attention was paid to low-dose effects of the cytotoxic drugs tested. To reflect this situation in vivo, multicellular tumor aggregates or "spheroids" of HepG2 cells were cultured and exposed to gamma irradiation alone or in combination with cisplatin for 4 h, gemcitabin for 4 or 24 h, or 5-fluorouracil for 4 h. In one experiment, the spheroids were cultured for 4 weeks in multiwell plates that allowed adhesion. Measurement of two-dimensional spheroid outgrowth was made every week for each spheroid. This kind of growth depends on the proliferation and motility of the cells that form the spheroid. In a second experiment, toxicity was evaluated by comparative growth curves by means of a three-dimensional growth assay and by histology. Supra-additive effects lasting for 4 weeks were observed for all drugs tested in combination with a gamma irradiation of 10 Gy.Key words: hepatocellular carcinoma, cisplatin, gemcitabine, 5-fluorouracil, gamma irradiation.

scholarly journals The Histone Variant MacroH2A1 Impacts Circadian Gene Expression and Cell Phenotype in an In Vitro Model of Hepatocellular Carcinoma

Biomedicines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 1057
Author(s):  
Annalucia Carbone ◽  
Elisabetta De Santis ◽  
Olga Cela ◽  
Vincenzo Giambra ◽  
Luca Miele ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
In Vitro Model ◽  
Epithelial To Mesenchymal Transition ◽  
Expression Patterns ◽  
Cell Phenotype ◽  
Alcoholic Fatty Liver ◽  
Mesenchymal Transition ◽  
Circadian Genes ◽  
Vitro Model

Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death worldwide. A foremost risk factor for HCC is obesity/metabolic syndrome-related non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH), which is prompted by remarkable changes in transcription patterns of genes enriching metabolic, immune/inflammatory, and circadian pathways. Epigenetic mechanisms play a role in NAFLD-associated HCC, and macroH2A1, a variant of histone H2A, is involved in the pathogenesis modulating the expression of oncogenes and/or tumor suppressor genes and interacting with SIRT1, which crucially impacts the circadian clock circuitry. Hence, we aimed to appraise if and how macroH2A1 regulated the expression patterns of circadian genes in the setting of NAFLD-associated HCC. We took advantage of an in vitro model of liver cancer represented by HepG2 (human hepatocarcinoma) cells stably knocked down for macroH2A1 and conducted whole transcriptome profiling and deep phenotyping analysis. We found up-regulation of PER1 along with several deregulated circadian genes, enriching several important pathways and functions related to cancer onset and progression, such as epithelial-to-mesenchymal transition, cell cycle deregulation, and DNA damage. PER1 silencing partially mitigated the malignant phenotype induced by the loss of macroH2A1 in HCC cells. In conclusion, our findings suggest a modulatory role for the core circadian protein PER1 in liver carcinogenesis in the context of a lack of the macroH2A1 epigenetic and transcriptional landscape.

scholarly journals Lactosylated Albumin Nanoparticles: Potential Drug Nanovehicles with Selective Targeting Toward an In Vitro Model of Hepatocellular Carcinoma

Molecules ◽  
2019 ◽  
Vol 24 (7) ◽  
pp. 1382 ◽  
Author(s):  
Nayelli Teran-Saavedra ◽  
Jose Sarabia-Sainz ◽  
Erika Silva-Campa ◽  
Alexel Burgara-Estrella ◽  
Ana Guzmán-Partida ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Chemical Structure ◽  
In Vitro Model ◽  
Ricinus Communis ◽  
Potential Drug ◽  
Albumin Nanoparticles ◽  
Selective Targeting ◽  
Vitro Model ◽  
Lectin Recognition

Hepatocellular carcinoma (HCC) ranks fifth in occurrence and second in mortality of all cancers. The development of effective therapies for HCC is urgently needed. Anticancer drugs targeted to the liver-specific asialoglycoprotein receptors (ASGPRs) are viewed as a promising potential treatment for HCC. ASGPRs facilitate the recognition and endocytosis of molecules, and possibly vehicles with galactose end groups, by the liver. In this study, bovine serum albumin (BSA) was conjugated with lactose using a thermal treatment. The formation of lactosylated BSA (BSA-Lac) was confirmed by a change of the chemical structure, increased molecular mass, and Ricinus communis lectin recognition. Subsequently, the low-crosslinking BSA-Lac nanoparticles (LC BSA-Lac NPs) and high-crosslinking BSA-Lac nanoparticles (HC BSA-Lac NPs) were synthesized. These nanoparticles presented spherical shapes with a size distribution of 560 ± 18.0 nm and 539 ± 9.0 nm, as well as an estimated surface charge of −26 ± 0.15 mV and −24 ± 0.45 mV, respectively. Both BSA-Lac NPs were selectively recognized by ASGPRs as shown by biorecognition, competition, and inhibition assays using an in vitro model of HCC. This justifies pursuing the strategy of using BSA-Lac NPs as potential drug nanovehicles with selective direction toward hepatocellular carcinoma.

An in vitro model for investigation of vitamin A effects on wound healing

2021 ◽  
pp. 1-6
Author(s):  
Hoda Keshmiri Neghab ◽  
Mohammad Hasan Soheilifar ◽  
Gholamreza Esmaeeli Djavid
Keyword(s):  
Wound Healing ◽  
Endothelial Cell ◽  
Vitamin A ◽  
In Vitro Model ◽  
Cellular Proliferation ◽  
Endothelial Cell Migration ◽  
Normal Fibroblast ◽  
Anti Inflammatory ◽  
Vitro Model

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inflammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inflammation responses.

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