Antitumoral Activity of Sorafenib in Hepatocellular Carcinoma: Effects on Cell Survival and Death Pathways, Cell Metabolism Reprogramming, and Nitrosative and Oxidative Stress

2016 ◽  
Vol 21 (5-6) ◽  
pp. 413-432 ◽  
Author(s):  
Francisco J. Molina-Ruiz ◽  
Raul Gonzalez ◽  
Maria A. Rodriguez-Hernandez ◽  
Elena Navarro-Villaran ◽  
Francisco J. Padillo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatocellular Carcinoma ◽  
Cell Survival ◽  
Cell Metabolism ◽  
Antitumoral Activity ◽  
And Oxidative Stress

scholarly journals Oxidative stress induces cell death partially by decreasing both mRNA and protein levels of nicotinamide phosphoribosyltransferase in differentiated PC12 cells

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e11401
Author(s):  
Cuiyan Zhou ◽  
Weihai Ying
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Cell Survival ◽  
Pc12 Cells ◽  
Neurological Diseases ◽  
Biological Effects ◽  
Stress Conditions ◽  
Nicotinamide Phosphoribosyltransferase ◽  
Differentiated Pc12 Cells ◽  
And Oxidative Stress

Background. Multiple studies have indicated crucial roles of NAD+ deficiency in several neurological diseases and aging. It is critical to discover the mechanisms underlying the NAD+ deficiency. A decreased level of Nicotinamide phosphoribosyltransferase (Nampt)—an important enzyme in the salvage pathway of NAD+ synthesis—has been found under certain pathological conditions, while the mechanisms underlying the Nampt decrease are unclear. The purpose of this study is to test the hypothesis that oxidative stress can produce decreased Nampt, and to investigate the biological effects of Nampt on NAD+ synthesis and cell survival under both basal and oxidative stress conditions. Methods. We used differentiated PC12 cells as a cellular model to investigate the effects of oxidative stress on the levels of Nampt. Multiple assays, including flow cytometry-based cell death assays and NAD+ assays were conducted. Results. First, oxidative stress can decrease the levels of Nampt mRNA and Nampt protein; second, Nampt plays significant roles in NAD+ synthesis under both basal conditions and oxidative stress conditions; third, Nampt plays critical roles in cell survival under both basal conditions and oxidative stress conditions; and fourth, oxidative stress produced decreased NAD+ levels and cell survival partially by decreasing Nampt. Collectively, our study has indicated that oxidative stress is a pathological factor leading to decreased Nampt, which plays important roles in oxidative stress-produced decreases in NAD+ levels and cell survival. Our findings have indicated major roles of Nampt in maintaining NAD+ levels and cell survival under both basal and oxidative stress conditions.

Phycocyanobilin promotes PC12 cell survival and modulates immune and inflammatory genes and oxidative stress markers in acute cerebral hypoperfusion in rats

2013 ◽  
Vol 272 (1) ◽  
pp. 49-60 ◽  
Author(s):  
Javier Marín-Prida ◽  
Nancy Pavón-Fuentes ◽  
Alexey Llópiz-Arzuaga ◽  
Julio R. Fernández-Massó ◽  
Liván Delgado-Roche ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Survival ◽  
Pc12 Cell ◽  
Cerebral Hypoperfusion ◽  
Oxidative Stress Markers ◽  
Inflammatory Genes ◽  
Stress Markers ◽  
And Oxidative Stress

scholarly journals Loss of protein targeting to glycogen sensitizes human hepatocellular carcinoma cells towards glucose deprivation mediated oxidative stress and cell death

2015 ◽  
Vol 35 (3) ◽  
Author(s):  
Rongqiang Yang ◽  
Mei Zhang ◽  
Amber Renee Gustafson ◽  
Eugenia Wang ◽  
Marsha Paulette Cole ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatocellular Carcinoma ◽  
Cell Death ◽  
Protein Targeting ◽  
Glucose Deprivation ◽  
Carcinoma Cells ◽  
Glycogen Accumulation ◽  
Liver Cancer Cells ◽  
Human Hepatocellular Carcinoma Cells ◽  
And Oxidative Stress

PTG is a protein that is critical for glycogen accumulation in various tissues such as the liver. Our present study shows that its loss sensitizes liver cancer cells towards metabolic and oxidative stress.

scholarly journals Molecular targets and oxidative stress biomarkers in hepatocellular carcinoma: an overview

2011 ◽  
Vol 9 (1) ◽  
pp. 171 ◽  
Author(s):  
Monica Marra ◽  
Ignazio M Sordelli ◽  
Angela Lombardi ◽  
Monica Lamberti ◽  
Luciano Tarantino ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatocellular Carcinoma ◽  
Molecular Targets ◽  
Oxidative Stress Biomarkers ◽  
Stress Biomarkers ◽  
And Oxidative Stress

scholarly journals Transforming Growth Factor-β and Oxidative Stress in Cancer: A Crosstalk in Driving Tumor Transformation

Cancers ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 3093
Author(s):  
Valeria Ramundo ◽  
Giuliana Giribaldi ◽  
Elisabetta Aldieri
Keyword(s):  
Oxidative Stress ◽  
Growth Factor ◽  
Cancer Cell ◽  
Transforming Growth Factor ◽  
Cell Metabolism ◽  
Transforming Growth Factor Β ◽  
Ros Production ◽  
Redox Imbalance ◽  
Cancer Cell Metabolism ◽  
And Oxidative Stress

Cancer metabolism involves different changes at a cellular level, and altered metabolic pathways have been demonstrated to be heavily involved in tumorigenesis and invasiveness. A crucial role for oxidative stress in cancer initiation and progression has been demonstrated; redox imbalance, due to aberrant reactive oxygen species (ROS) production or deregulated efficacy of antioxidant systems (superoxide dismutase, catalase, GSH), contributes to tumor initiation and progression of several types of cancer. ROS may modulate cancer cell metabolism by acting as secondary messengers in the signaling pathways (NF-kB, HIF-1α) involved in cellular proliferation and metastasis. It is known that ROS mediate many of the effects of transforming growth factor β (TGF-β), a key cytokine central in tumorigenesis and cancer progression, which in turn can modulate ROS production and the related antioxidant system activity. Thus, ROS synergize with TGF-β in cancer cell metabolism by increasing the redox imbalance in cancer cells and by inducing the epithelial mesenchymal transition (EMT), a crucial event associated with tumor invasiveness and metastases. Taken as a whole, this review is addressed to better understanding this crosstalk between TGF-β and oxidative stress in cancer cell metabolism, in the attempt to improve the pharmacological and therapeutic approach against cancer.

scholarly journals Mechanistic Insights into Oxidative Stress and Apoptosis Mediated by Tannic Acid in Human Liver Hepatocellular Carcinoma Cells

2019 ◽  
Vol 20 (24) ◽  
pp. 6145 ◽  
Author(s):  
Priscilla Mhlanga ◽  
Pearl O. Perumal ◽  
Anou M. Somboro ◽  
Daniel G. Amoako ◽  
Hezekiel M. Khumalo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatocellular Carcinoma ◽  
Cell Death ◽  
Dna Fragmentation ◽  
Tannic Acid ◽  
Hepg2 Cells ◽  
Human Liver ◽  
Dna Integrity ◽  
Liver Hepatocellular Carcinoma ◽  
And Oxidative Stress

The study investigated the cytotoxic effect of a natural polyphenolic compound Tannic acid (TA) on human liver hepatocellular carcinoma (HepG2) cells and elucidated the possible mechanisms that lead to apoptosis and oxidative stress HepG2 cell. The HepG2 cells were treated with TA for 24 h and various assays were conducted to determine whether TA could induce cell death and oxidative stress. The cell viability assay was used to determine the half maximal inhibitory concentration (IC50), caspase activity and cellular ATP were determined by luminometry. Microscopy was employed to determine deoxyribonucleic acid (DNA) integrity, while thiobarbituric acid (TBARS) and nitric oxide synthase (NOS) assays were used to elucidate cellular reactive oxygen species (ROS) and reactive nitrogen species (RNS), respectively. Western blotting was used to confirm protein expression. The results revealed that tannic acid induced caspase activation and increased the presence of cellular ROS and RNS, while downregulating antioxidant expression. Tannic acid also showed increased cell death and increased DNA fragmentation. In conclusion, TA was able to induce apoptosis by DNA fragmentation via caspase-dependent and caspase-independent mechanism. It was also able to induce oxidative stress, consequently contributing to cell death.

scholarly journals Potential Role of Microfibrillar-Associated Protein 4, Fibrotic Indices and Oxidative Stress in Hepatocellular Carcinoma

2018 ◽  
Vol 86 (4) ◽  
pp. 44 ◽  
Author(s):  
Mohamed Salama ◽  
Manal Nomir ◽  
Maryan Fahmi ◽  
Amal El-Gayar ◽  
Mamdouh El-Shishtawy
Keyword(s):  
Oxidative Stress ◽  
Hepatocellular Carcinoma ◽  
Potential Role ◽  
Control Group ◽  
Significant Elevation ◽  
Cirrhotic Patients ◽  
Mechanisms Of Persistence ◽  
And Oxidative Stress ◽  
Related Mortality

Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related mortality worldwide. In an attempt to understand some potential mechanisms of persistence and oncogenicity of Hepatitis C virus (HCV)-related HCC, microfibrillar-associated protein 4 (MFAP4), fibrotic indices and oxidative status biomarkers were assessed in the sera of 50 patients with HCV-associated HCC, 25 patients with HCV-related liver cirrhosis and 15 healthy individuals. Serum oxidized Coenzyme Q10 (CoQ10) and malondialdehyde showed significant elevation in HCC patients compared to the control group (p < 0.001), as well as cirrhotic patients (p < 0.05 and p < 0.001, respectively), while serum glutathione content and superoxide dismutase activity were significantly decreased in HCC patients compared to the control group (p < 0.001). Serum MFAP4, aspartate aminotransferase to platelet ratio index (APRI), fibrosis index based on the 4 factors (FIB-4) and Forns index showed significant increase in HCC patients compared to the control group (p < 0.001), while only APRI and FIB-4 were significantly different between HCC and cirrhotic patients (p < 0.05), with a sensitivity of 86% and 92%, respectively, at cut off ≥0.7 for APRI and ≥1.57 for FIB-4. Therefore, increasing oxidative stress and fibrosis might mediate HCV induced cirrhosis and HCC. APRI and FIB-4 may be used as a simple non-expensive formula for the screening of HCC rather than MFAP4.

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