Allyl-isatin suppresses cell viability, induces cell cycle arrest, and promotes cell apoptosis in hepatocellular carcinoma HepG2 cells

2016 ◽  
Vol 30 (3) ◽  
pp. 253-262 ◽  
Author(s):  
Weihua Bian ◽  
Yukuan An ◽  
Huiqing Qu ◽  
Yue Yang ◽  
Junhou Yang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cell Viability ◽  
Cell Cycle Arrest ◽  
Cell Apoptosis ◽  
Hepg2 Cells ◽  
Cycle Arrest

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

scholarly journals Alpha7 Nicotinic Acetylcholine Receptor Mediates Nicotine-induced Apoptosis and Cell Cycle Arrest of Hepatocellular Carcinoma HepG2 Cells

2019 ◽  
Vol 10 (1) ◽  
pp. 65-71 ◽  
Author(s):  
Khalil Hajiasgharzadeh ◽  
Mohammad Hossein Somi ◽  
Behzad Mansoori ◽  
Mohammad Amin Doustvandi ◽  
Fatemeh Vahidian ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cell Viability ◽  
Nicotinic Acetylcholine Receptor ◽  
Hepg2 Cells ◽  
Nicotinic Acetylcholine ◽  
Alpha7 Nicotinic Acetylcholine Receptor ◽  
Qrt Pcr ◽  
Cycle Arrest ◽  
Induced Apoptosis

Purpose: The cytotoxic properties upon treatment with nicotine have been reported in several studies, but the underlying mechanisms remain not fully defined. The alpha7 nicotinic acetylcholine receptor (α7nAChR) is one of the important nicotinic receptors, which nicotine partly by binding to this receptor exerts its effects. The current study aimed to investigates the influences of nicotine on cellular proliferative and apoptotic activities and tried to determine the involvement of α7nAChR in these functions. Methods: Human hepatocellular carcinoma (HepG2) cell line was used to determine the individual or combined effects of treatments with nicotine (10 μM) and specific siRNA (100 nM) targeting α7nAChR expression. The MTT assay, DAPI staining assay, and flow cytometry assay were applied to measure the cell viability, apoptosis and cell cycle progression of the cells, respectively. In addition, the changes in the mRNA level of the genes were assessed by qRT-PCR. Results: Compared to control groups, the cells treated with nicotine exhibited significant dosedependent decreases in cell viability (log IC50 = -5.12±0.15). Furthermore, nicotine induced apoptosis and cell cycle arrest especially at G2/M Phase. The qRT-PCR revealed that nicotine increased the mRNA levels of α7nAChR as well as caspase-3 and suppressed the expression of cyclin B1. Treatment with α7-siRNA abolished these effects of nicotine. Conclusion: These experiments determined that upregulation of α7nAChR by nicotine inhibits HepG2 cells proliferation and induces their apoptosis. These effects blocked by treatment with α7-siRNA, which indicates the involvement of α7nAChR pathways in these processes.

scholarly journals Nomad Jellyfish Rhopilema nomadica Venom Induces Apoptotic Cell Death and Cell Cycle Arrest in Human Hepatocellular Carcinoma HepG2 Cells

Molecules ◽  
2021 ◽  
Vol 26 (17) ◽  
pp. 5185
Author(s):  
Mohamed M. Tawfik ◽  
Nourhan Eissa ◽  
Fayez Althobaiti ◽  
Eman Fayad ◽  
Ali H. Abu Almaaty
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Dna Fragmentation ◽  
Hepg2 Cells ◽  
Apoptotic Cell ◽  
Cycle Arrest ◽  
Jellyfish Venom

Jellyfish venom is a rich source of bioactive proteins and peptides with various biological activities including antioxidant, antimicrobial and antitumor effects. However, the anti-proliferative activity of the crude extract of Rhopilema nomadica jellyfish venom has not been examined yet. The present study aimed at the investigation of the in vitro effect of R. nomadica venom on liver cancer cells (HepG2), breast cancer cells (MDA-MB231), human normal fibroblast (HFB4), and human normal lung cells (WI-38) proliferation by using MTT assay. The apoptotic cell death in HepG2 cells was investigated using Annexin V-FITC/PI double staining-based flow cytometry analysis, western blot analysis, and DNA fragmentation assays. R. nomadica venom displayed significant dose-dependent cytotoxicity on HepG2 cells after 48 h of treatment with IC50 value of 50 μg/mL and higher toxicity (3:5-fold change) against MDA-MB231, HFB4, and WI-38 cells. R. nomadica venom showed a prominent increase of apoptosis as revealed by cell cycle arrest at G2/M phase, upregulation of p53, BAX, and caspase-3 proteins, and the down-regulation of anti-apoptotic Bcl-2 protein and DNA fragmentation. These findings suggest that R. nomadica venom induces apoptosis in hepatocellular carcinoma cells. To the best of the authors’ knowledge, this is the first scientific evidence demonstrating the induction of apoptosis and cell cycle arrest of R. nomadica jellyfish venom.

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