Phenylarsine oxide (PAO) induces apoptosis in HepG2 cellsviaROS-mediated mitochondria and ER-stress dependent signaling pathways

Metallomics ◽  
2017 ◽  
Vol 9 (12) ◽  
pp. 1756-1764 ◽  
Author(s):  
Ping Huang ◽  
Yu Hua Zhang ◽  
Xiao Wei Zheng ◽  
Yu Jia Liu ◽  
Hong Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Er Stress ◽  
Signaling Pathways ◽  
Hepg2 Cells ◽  
Human Hepatocellular Carcinoma ◽  
Phenylarsine Oxide ◽  
Cytotoxic Effects ◽  
Stress Dependent

PAO showed potent cytotoxic effects on arsenic resistant human hepatocellular carcinoma HepG2 cells by producing ROS.

scholarly journals Role of the Death Receptor and Endoplasmic Reticulum Stress Signaling Pathways in Polyphyllin I-Regulated Apoptosis of Human Hepatocellular Carcinoma HepG2 Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Qihui Luo ◽  
Dandan Yang ◽  
Qi Qi ◽  
Chao Huang ◽  
Bing Chen ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Er Stress ◽  
Signaling Pathways ◽  
Hepg2 Cells ◽  
Death Receptor ◽  
Receptor Signaling ◽  
Death Receptor Signaling

Polyphyllin has been reported to exhibit anticancer effects against various types of cancer via the proapoptotic signaling pathway. The aim of the present study was to investigate the role of the endoplasmic reticulum stress and death receptor signaling pathways in PPI-induced apoptosis of human hepatocellular carcinoma HepG2 cells. Analysis demonstrated that PPI could significantly inhibit the proliferation and induce apoptosis of HepG2 cells in a dose- and time-dependent manner. Investigation into the molecular mechanism of PPI indicated that PPI notably mediated ER stress activation via IRE-1 overexpression and activation of the caspase-12 to protect HepG2 cells against apoptosis. In addition, PPI markedly induced the expression of death receptors signaling pathways-associated factors, including tumor necrosis factor (TNF) receptor 1/TNF-αand FAS/FASL. Additionally, suppression of the death receptor signaling pathways with a caspase-8 inhibitor, Z-IETD-FMK, revealed an increase in the death rate and apoptotic rate of HepG2 cells. Collectively, the findings of the present study suggested that the ER stress and death receptor signaling pathways were associated with PPI-induced HepG2 cell apoptosis; however, endoplasmic reticulum stress may serve a protective role in this process. The combination of PPI and Z-IETD-FMK may activate necroptosis, which enhances apoptosis. Therefore, the results of the present study may improve understanding regarding the roles of signaling pathways in PPI regulated apoptosis and contribute to the development of novel therapies for the treatment of HCC.

Effects of Copper Nanoparticles on mRNA and Small RNA Expression in Human Hepatocellular Carcinoma (HepG2) Cells

2021 ◽  
Vol 21 (10) ◽  
pp. 5083-5098
Author(s):  
Sheau-Fung Thai ◽  
Carlton P. Jones ◽  
Brian L. Robinette ◽  
Hongzu Ren ◽  
Beena Vallant ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Signaling Pathways ◽  
Copper Nanoparticles ◽  
Hepg2 Cells ◽  
Human Hepatocellular Carcinoma ◽  
Phase Iii ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Nuclear Factor ◽  
Protein Ubiquitination

With the advancement of nanotechnology, nanoparticles are widely used in many different industrial processes and consumer products. Copper nanoparticles (Cu NPs) are among the most toxic nanomaterials. We investigated Cu NPs toxicity in Human Hepatocellular carcinoma (HepG2) cells by examining signaling pathways, and microRNA/mRNA interactions. We compared the effects of exposures to Cu NPs at various concentrations and CuCl2 was used as a control. The number of differentially expressed mRNA did not follow a linear dose-response relationship for either Cu NPs or CuCl2 treatments. The most significantly altered genes and pathways by Cu NPs exposure were NRF2 (nuclear factor erythroid 2 related factor 2)-mediated oxidative stress response, protein ubiquitination, Tumor protein p53 (p53), phase I and II metabolizing enzymes, antioxidant proteins and phase III detoxifying gene pathways.Messenger RNA-microRNA interaction from MicroRNA Target Filter Analyses revealed more signaling pathways altered in Cu NPs treated samples than transcriptomics alone, including cell proliferation, DNA methylation, endoplasmic reticulum (ER) stress, apoptosis, autophagy, reactive oxygen species, inflammation, tumorigenesis, extracellular matrix/angiogenesis and protein synthesis. In contrast, in the control (CuCl2) treated samples showed mostly changes in inflammation mainly through regulation of the Nuclear Factor Kappa-light-chain-enhancer of Activated B-cells (NFκB). Further, some RNA based parameters that showed promise as biomarkers of Cu NPs exposure including both well and lesser known genes: heme oxygenase 1 (HMOX1), heat shock protein, c-Fos proto-oncogene, DNA methyltransferases, and glutamate-cysteine ligase modifier subunit (GCLM, part of the glutathione synthesis pathway). The differences in signaling pathways altered by the Cu NPs and CuCl2 treatments suggest that the effects of the Cu NPs were not the results of nanomaterial dissolution to soluble copper ions.

Ellipticine induces apoptosis through p53-dependent pathway in human hepatocellular carcinoma HepG2 cells

Life Sciences ◽  
2006 ◽  
Vol 78 (22) ◽  
pp. 2550-2557 ◽  
Author(s):  
Yu-Chun Kuo ◽  
Po-Lin Kuo ◽  
Ya-Ling Hsu ◽  
Chien-Yu Cho ◽  
Chun-Ching Lin
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepg2 Cells ◽  
Human Hepatocellular Carcinoma ◽  
Dependent Pathway

The Effect and Mechanism of Apoptosis Induced by Desacetylcinobufotalin (DEBF) in Human Hepatocellular Carcinoma HepG2 Cells

2013 ◽  
Vol 395-396 ◽  
pp. 587-590
Author(s):  
Xu Chao ◽  
Lin Dang ◽  
Min Hui Wei
Keyword(s):  
Hepatocellular Carcinoma ◽  
Antitumor Activity ◽  
Western Blot ◽  
Hepg2 Cells ◽  
Human Hepatocellular Carcinoma ◽  
Inhibition Effect ◽  
Marked Inhibition ◽  
Mitochondria Pathway

The cytotoxicity of Desacetylcinobufotalin (DEBF) and apoptosis induced by DEBF was measured. Additionally the mechanism of Apoptosis induced by DEBF was studied through Western blot. The results show DEBF displayed the marked inhibition effect to HepG2 cells and the IC50value is 0.0279μmol/ml. The expression of Bax was significantly increased and the expression of Bcl-2 was markedly decreased, compared to the control. The data suggest DEBF had significant antitumor activity through induction apoptosis via mitochondria pathway.

scholarly journals Deoxynivalenol downregulates NRF2-induced cytoprotective response in human hepatocellular carcinoma (HepG2) cells

Toxicon ◽  
2021 ◽  
Vol 193 ◽  
pp. 4-12
Author(s):  
Siqiniseko Ndlovu ◽  
Savania Nagiah ◽  
Naeem Sheik Abdul ◽  
Terisha Ghazi ◽  
Anil A. Chuturgoon
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepg2 Cells ◽  
Human Hepatocellular Carcinoma ◽  
Cytoprotective Response
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