Micronucleus induction and cell cycle alterations produced by deoxynivalenol and its acetylated derivatives in individual and combined exposure on HepG2 cells

2018 ◽  
Vol 118 ◽  
pp. 719-725 ◽  
Author(s):  
Ana Juan-García ◽  
Mercedes Taroncher ◽  
Guillermina Font ◽  
María-José Ruiz
Keyword(s):  
Cell Cycle ◽  
Hepg2 Cells ◽  
Combined Exposure ◽  
Micronucleus Induction ◽  
Cell Cycle Alterations

Induction of Apoptosis by Nano‐Synthesized Complexes of H2L and its Cu(II) Complex in Human Hepatocellular Carcinoma Cells

2020 ◽  
Vol 20 ◽  
Author(s):  
Thoria Diab ◽  
Tarek M. Mohamed ◽  
Alaa Hamed ◽  
Mohamed Gaber
Keyword(s):  
Cell Cycle ◽  
Metal Complexes ◽  
Hepg2 Cells ◽  
Therapeutic Potential ◽  
Free Ligand ◽  
Organometallic Complexes ◽  
Phase Cell ◽  
Sod Activity ◽  
Induced Apoptosis

Background: Chemotherapy is currently the most utilized treatment for cancer. Therapeutic potential of metal complexes in cancer therapy has attracted a lot of interest. The mechanisms of action of most organometallic complexes are poorly understood. Objective: This study was designed to explore the mechanisms governing the anti-proliferative effect of the free ligand N1,N6‐bis((2‐hydroxynaphthalin‐1‐yl)methinyl)) adipohydrazone (H2L) and its complexes of Mn(II), Co(II), Ni(II) and Cu(II). Methods: Cells were exposed to H2L or its metal complexes where cell viability determined by MTT assay. Cell cycle was analysed by flow cytometry. In addition, qRT-PCR was used to monitor the expression of Bax and Bcl-2. Moreover, molecular docking was carried out to find the potentiality of Cu(II) complex as an inhibitor of Adenosine Deaminase (ADA). ADA, Superoxide Dismutase (SOD) and reduced Glutathione (GSH) levels were measured in the most affected cancer cell line. Results: The obtained results demonstrated that H2L and its Cu(II) complex exhibited a strong cytotoxic activity compared to other complexes against HepG2 cells (IC50 = 4.14±0.036μM/ml and 3.2±0.02μM/ml), respectively. Both H2L and its Cu(II) complex induced G2/M phase cell cycle arrest in HepG2 cells. Additionally, they induced apoptosis in HepG2 cells via upregulation of Bax and downregulation of Bcl-2. Interestingly, the activity of ADA was decreased by 2.8 fold in HepG2 cells treated with Cu(II) complex compared to untreated cells. An increase of SOD activity and GSH level in HepG2 cells compared to control was observed. Conclusion: The results concluded that Cu(II) complex of H2L induced apoptosis in HepG2 cells. Further studies are needed to confirm its anti-cancer effect in vivo.

Hydrogen peroxide and quercetin induced changes on cell viability, apoptosis and oxidative stress in HepG2 cells

2020 ◽  
Vol 01 ◽  
Author(s):  
Ayşe Mine Yılmaz ◽  
Gökhan Biçim ◽  
Kübra Toprak ◽  
Betül Karademir Yılmaz ◽  
Irina Milisav ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Hydrogen Peroxide ◽  
Cell Viability ◽  
Hepg2 Cells ◽  
Proteasome Activity ◽  
Cell Cycle Phases ◽  
Induced Changes ◽  
And Oxidative Stress ◽  
Quercetin Treatment

Background: Different cellular responses influence the progress of cancer. In this study, we have investigated the effect of hydrogen peroxide and quercetin induced changes on cell viability, apoptosis and oxidative stress in human hepatocellular carcinoma (HepG2) cells. Methods: The effects of hydrogen peroxide and quercetin on cell viability, cell cycle phases and oxidative stress related cellular changes were investigated. Cell viability was assessed by WST-1 assay. Apoptosis rate, cell cycle phase changes and oxidative stress were measured by flow cytometry. Protein expressions of p21, p27, p53, NF-Kβ-p50 and proteasome activity were determined by Western blot and fluorometry, respectively. Results: Hydrogen peroxide and quercetin treatment resulted in decreased cell viability and increased apoptosis in HepG2 cells. Proteasome activity was increased by hydrogen peroxide but decreased by quercetin treatment. Conclusion: Both agents resulted in decreased p53 protein expression and increased cell death by different mechanisms regarding proteostasis and cell cycle phases.

Evaluation of NovelN-(piperidine-4-yl)benzamide Derivatives as Potential Cell Cycle Inhibitors in HepG2 Cells

2014 ◽  
Vol 86 (2) ◽  
pp. 223-231 ◽  
Author(s):  
Jin Hou ◽  
Wei Zhao ◽  
Zhi-Ning Huang ◽  
Shao-Mei Yang ◽  
Li-Juan Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Hepg2 Cells ◽  
Cell Cycle Inhibitors ◽  
Benzamide Derivatives

NCPMF-60 induces G2/M cell cycle arrest and apoptosis in human hepatocellular carcinoma HepG2 cells

2011 ◽  
Vol 22 (1) ◽  
pp. 46-57 ◽  
Author(s):  
Qin-Sheng Dai ◽  
Wei Liu ◽  
Xiao-Bing Wang ◽  
Na Lu ◽  
Dan-Dan Gong ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Hepg2 Cells ◽  
Human Hepatocellular Carcinoma ◽  
M Cell ◽  
Cycle Arrest

Induction of UGT1A1 and CYP2B6 by an Antimitogenic Factor in HepG2 Cells Is Mediated through Suppression of Cyclin-Dependent Kinase 2 Activity: Cell Cycle-Dependent Expression

2009 ◽  
Vol 38 (1) ◽  
pp. 177-186 ◽  
Author(s):  
Junko Sugatani ◽  
Makoto Osabe ◽  
Masatoshi Kurosawa ◽  
Naomi Kitamura ◽  
Akira Ikari ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Hepg2 Cells ◽  
Cyclin Dependent Kinase ◽  
Cycle Dependent

Retinoic acid modulates the cell-cycle in fetal rat hepatocytes and HepG2 cells by regulating cyclin-cdk activities

2003 ◽  
Vol 23 (3) ◽  
pp. 179-186 ◽  
Author(s):  
A. Alisi ◽  
Silvia Leoni ◽  
A. Piacentani ◽  
L. Conti Devirgiliis
Keyword(s):  
Cell Cycle ◽  
Retinoic Acid ◽  
Hepg2 Cells ◽  
Rat Hepatocytes ◽  
Fetal Rat
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