Search results for "Programmed cell death"
showing 10 items of 609 documents
Extracellular Vesicles and Tumor-Immune Escape: Biological Functions and Clinical Perspectives
2020
The modulation of the immune system is one of the hallmarks of cancer. It is now widely described that cancer cells are able to evade the immune response and thus establish immune tolerance. The exploration of the mechanisms underlying this ability of cancer cells has always attracted the scientific community and is the basis for the development of new promising cancer therapies. Recent evidence has highlighted how extracellular vesicles (EVs) represent a mechanism by which cancer cells promote immune escape by inducing phenotypic changes on different immune cell populations. In this review, we will discuss the recent findings on the role of tumor-derived extracellular vesicles (TEVs) in re…
Glutathione in Cancer Cell Death
2011
Glutathione (L-γ-glutamyl-L-cysteinyl-glycine; GSH) in cancer cells is particularly relevant in the regulation of carcinogenic mechanisms; sensitivity against cytotoxic drugs, ionizing radiations, and some cytokines; DNA synthesis; and cell proliferation and death. The intracellular thiol redox state (controlled by GSH) is one of the endogenous effectors involved in regulating the mitochondrial permeability transition pore complex and, in consequence, thiol oxidation can be a causal factor in the mitochondrion-based mechanism that leads to cell death. Nevertheless GSH depletion is a common feature not only of apoptosis but also of other types of cell death. Indeed rates of GSH synthesis and…
Colorectal Cancer Stem Cells and Cell Death
2011
Nowadays it is reported that, similarly to other solid tumors, colorectal cancer is sustained by a rare subset of cancer stem-like cells (CSCs), which survive conventional anticancer treatments, hanks to efficient mechanisms allowing escape from apoptosis, triggering tumor recurrence. To improve patient outcomes, conventional anticancer therapies have to be replaced with specific approaches targeting CSCs. In this review we provide strong support that BMP4 is an innovative therapeutic approach to prevent colon cancer growth increasing differentiation markers expression and apoptosis. Recent data suggest that in colorectal CSCs, protection from apoptosis is achieved by interleukin-4 (IL-4) a…
Deglycosylated bleomycin triggers apoptosis in laryngeal carcinoma cells in a caspase and reactive oxygen species independent manner
2008
Background: Bleomycin-A2, a member of a family of glycopeptide antibiotics, has potent antitumor activity against a range of lymphomas, head and neck cancer and germ cell tumors. However, little is known about the biologic activity of the carbohydrate moiety in Bleomycin-A2-induced cytotoxicity. Methods: We compared the capacity of Bleomycin-A2 and its deglycosylated form (deglycoBleomycin-A2) to induce cell death. Apoptosis was analyzed by cell nuclear staining with Hoechst 33342 dye and DNA fragmentation. The signal transduction pathway was measured through Western blotting and production of reactive oxygen species (ROS). Results: When tested on HEp-2 laryngeal carcinoma cells, Bleomyc…
Interplays between nitric oxide and reactive oxygen species in cryptogein signalling
2014
The cellular messenger nitric oxide (NO) has many functions in plants. In this study, we investigated its interplays with Reactive Oxygen Species (ROS) in the defense responses triggered by the elicitin cryptogein produced by the oomycete Phytophthora cryptogea. The production of NO induced by cryptogein in tobacco cell suspensions was partly regulated through a ROS-dependent pathway involving the NADPH oxidase NtRBOHD. In turn, NO down-regulated the level of H2O2 derived from NtRBOHD activity. Both NO and ROS synthesis appeared to be under the control of two redundant isoforms of histone deacetylases of type 2 acting as negative regulators of cell death. Occurrence of an interplay between …
Mitochondrial oxidative stress and CD95 ligand: A dual mechanism for hepatocyte apoptosis in chronic alcoholism
2002
Apoptosis plays an important role in the progression of alcohol-induced liver disease to cirrhosis. Oxidative stress is an early event in the development of apoptosis. The major aim of this study was to study the conditions in which oxidative stress occurs in chronic alcoholism and its relationship with apoptosis of hepatocytes. We have found that oxidative stress is associated with chronic ethanol consumption in humans and in rats, in the former independently of the existence of alcohol-induced liver disease. Ethanol or acetaldehyde induces apoptosis in hepatocytes isolated from alcoholic rats, but not in those from control rats. Inhibition of aldehyde dehydrogenase, but not of cytochrome …
The Relationship between Alcohol–induced Apoptosis and Oxidative Stress in the Liver
2005
This chapter discusses the relationship of apoptosis and oxidative stress induced by alcohol in the liver. Oxidative stress is involved in the pathogenesis and progression of alcohol-induced liver disease. Chronic alcoholism always causes oxidative stress independently of the presence of liver disease. Two key mechanisms are responsible for it: (1) the mitochondrial respiratory chain and (2) cytochrome P450 2El activity. Increased production of reactive oxygen species at complexes I and III together with NADH overproduction would be the major cause for mitochondrial oxidative stress in chronic alcoholism. Reactive Oxygen Species (ROS) cause oxidative damage, which may lead to cell death by …
17β-Estradiol-dependent regulation of chaperone expression and telomerase activity in the marine sponge Geodia cydonium
1999
It is known that species belonging to the lowest metazoan phylum, the Porifera (sponges), do not develop tumors. Sponge cells share with tumor cells of higher animals at least one characteristic; they contain high levels of telomerase activity, suggesting that they possess a high proliferation capacity. This assumption, however, has not been substantiated experimentally. In addition, sponges show a specific bauplan, leading us to postulate that they undergo apoptosis to replace a given set of cells at a given time. In the present study, 17β-estradiol (βE2) was used as a defined agent to assess its effect on both the telomerase activity and the process of apoptosis in the marine sponge Geodi…
Oxidative stress in diabetic retinopathy
2020
Diabetic retinopathy (DR) is the leading cause of acquired blindness in working adults worldwide. Biochemical changes in DR contribute to both the microscopic structural and functional changes in the retina. All these alterations result in retinal damage that can be assessed by funduscopy, optical coherence tomography (OCT), and angioOCT. Reactive oxygen species (ROS) overproduction in the mitochondria is considered a causal link between elevated glucose and biochemical abnormalities in the pathophysiology of DR. Moreover, oxidative-induced pathways also seem to provide positive feedback to ROS production, resulting in a vicious cycle. ROS can directly damage lipids, proteins, and DNA, lead…
Diabetic Retinopathy and Oxidative Stress
2014
Abstract Diabetic retinopathy (DR) is the leading cause of acquired blindness in working age adults worldwide. Biochemical changes in DR contribute to both the microscopic structural and functional changes in the retina. All these alterations result in macroscopic retinal damage that can be assessed by funduscopy. The overproduction of reactive oxygen species (ROS) in the mitochondria is considered a causal link between elevated glucose and biochemical abnormalities in the pathophysiology of DR. Moreover, oxidatively induced pathways also seem to provide positive feedback to ROS production, resulting in a vicious cycle. ROS can directly damage lipids, proteins and DNA, leading to cell death…