scholarly journals Pyroptosis, a New Breakthrough in Cancer Treatment

2021 ◽  
Vol 11 ◽  
Author(s):  
Dengqiang Wu ◽  
Changhong Wei ◽  
Yujie Li ◽  
Xuejia Yang ◽  
Sufang Zhou
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Inflammatory Response ◽  
Cancer Treatment ◽  
Tumor Markers ◽  
Therapeutic Targets ◽  
Protein Family ◽  
Cell Necrosis ◽  
Clinical Cancer ◽  
The Relationship

The way of cell death can be roughly divided into two categories: cell necrosis and PCD(programmed cell death). Pyroptosis is a kind of PCD, its occurrence depends on the gasdermin protein family and it will produce inflammatory response. With constant research in recent years, more and more evidences show that pyroptosis is closely related to the occurrence and development of tumors. The treatment of tumors is a big problem worldwide. We focus on whether we can discover new potential tumor markers and new therapeutic targets from the mechanism. If we can understand the mechanism of pyroptosis and clear the relationship between pyroptosis and the development of tumors, this may provide a new reference for clinical cancer treatment.

scholarly journals Initiation and Execution of Programmed Cell Death and Regulation of Reactive Oxygen Species in Plants

2021 ◽  
Vol 22 (23) ◽  
pp. 12942
Author(s):  
Chanjuan Ye ◽  
Shaoyan Zheng ◽  
Dagang Jiang ◽  
Jingqin Lu ◽  
Zongna Huang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Plant Stress ◽  
Reactive Oxygen ◽  
Signalling Pathways ◽  
Oxygen Species ◽  
Signalling Molecules ◽  
Plant Stress Tolerance ◽  
The Relationship

Programmed cell death (PCD) plays crucial roles in plant development and defence response. Reactive oxygen species (ROS) are produced during normal plant growth, and high ROS concentrations can change the antioxidant status of cells, leading to spontaneous cell death. In addition, ROS function as signalling molecules to improve plant stress tolerance, and they induce PCD under different conditions. This review describes the mechanisms underlying plant PCD, the key functions of mitochondria and chloroplasts in PCD, and the relationship between mitochondria and chloroplasts during PCD. Additionally, the review discusses the factors that regulate PCD. Most importantly, in this review, we summarise the sites of production of ROS and discuss the roles of ROS that not only trigger multiple signalling pathways leading to PCD but also participate in the execution of PCD, highlighting the importance of ROS in PCD.

scholarly journals Bcl2 inhibits apoptosis associated with terminal differentiation of HL- 60 myeloid leukemia cells

Blood ◽  
1994 ◽  
Vol 83 (8) ◽  
pp. 2261-2267 ◽  
Author(s):  
L Naumovski ◽  
ML Cleary
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Myeloid Cells ◽  
Terminal Differentiation ◽  
Retroviral Gene Transfer ◽  
Protein Levels ◽  
All Trans Retinoic Acid ◽  
Bcl2 Protein ◽  
The Relationship

Abstract The Bcl2 protein inhibits apoptosis (programmed cell death) induced by a variety of noxious stimuli. However, relatively little is known about its effect on apoptosis that occurs after terminal differentiation. Bcl2 protein levels decrease during differentiation of myeloid cells into granulocytes that subsequently undergo apoptosis, but the potential role of Bcl2 in coupling survival and differentiation remains undefined. To ascertain the relationship between decreasing Bcl2 levels and the onset of apoptosis in differentiating myeloid cells, Bcl2 was hyperexpressed in the HL-60 cell line after retroviral gene transfer. After treatment of HL-60/BCL2 cells with all-trans retinoic acid or phorbol myristic acid, Bcl2 levels did not decrease as in normal HL-60 cells but, rather, increased because of activation of the viral promoter. Differentiation of the Bcl2-overexpressing cells was similar to that of normal HL-60 cells, but they showed little evidence for apoptosis and had a prolonged survival. These studies show that the survival-enhancing properties of Bcl2 counteract programmed cell death that accompanies terminal differentiation; however, Bcl2 has no significant effect on differentiation itself, suggesting that apoptosis and differentiation are regulated independently in myeloid cells.

scholarly journals MicroRNA (miRNA)-to-miRNA Regulation of Programmed Cell Death 4 (PDCD4)

2019 ◽  
Vol 39 (18) ◽  
Author(s):  
Pamela Ajuyah ◽  
Meredith Hill ◽  
Alireza Ahadi ◽  
Jing Lu ◽  
Gyorgy Hutvagner ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Suppressor ◽  
Programmed Cell Death ◽  
Tumor Suppressor Genes ◽  
Untranslated Region ◽  
Inhibitory Concentration ◽  
Mutational Analysis ◽  
Mirna Regulation ◽  
Programmed Cell Death 4 ◽  
The Relationship

ABSTRACT The regulation of tumor suppressor genes by microRNAs (miRNAs) is often demonstrated as a one-miRNA-to-one-target relationship. However, given the large number of miRNA sites within a 3′ untranslated region (UTR), most targets likely undergo miRNA cooperation or combinatorial action. Programmed cell death 4 (PDCD4), an important tumor suppressor, prevents neoplastic events and is commonly downregulated in cancer. This study investigates the relationship between miRNA 21 (miR-21) and miR-499 in regulating PDCD4. This was explored using miRNA overexpression, mutational analysis of the PDCD4 3′ UTR to assess regulation at each miRNA site, and 50% inhibitory concentration (IC50) calculations for combinatorial behavior. We demonstrate that the first miR-499 binding site within PDCD4 is inactive, but the two remaining sites are both required for PDCD4 suppression. Additionally, the binding of miR-21 to PDCD4 influenced miR-499 activity through an increase in its silencing potency and stabilization of its mature form. Furthermore, adjoining miRNA sites more than 35 nucleotides (nt) apart could potentially regulate thousands of 3′ UTRs, similar to that observed between miR-21 and miR-499. The regulation of PDCD4 serves as a unique example of regulatory action by multiple miRNAs. This relationship was predicted to occur on thousands of targets and may represent a wider mode of miRNA regulation.

scholarly journals Association between Programmed Cell Death 6 Interacting Protein Insertion/Deletion Polymorphism and the Risk of Breast Cancer in a Sample of Iranian Population

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Mohammad Hashemi ◽  
Javad Yousefi ◽  
Seyed Mehdi Hashemi ◽  
Shadi Amininia ◽  
Mahboubeh Ebrahimi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Case Control Study ◽  
Iranian Population ◽  
Interacting Protein ◽  
Apoptosis Pathway ◽  
Protein Insertion ◽  
The Relationship ◽  
Control Study

It has been suggested that genetic factors contribute to patients’ vulnerability to breast cancer (BC). The programmed cell death 6 interacting protein (PDCD6IP) encodes for a protein that is known to bind to the products of the PDCD6 gene, which is involved in the apoptosis pathway. The aim of this case-control study is to investigate the relationship between thePDCD6IP15 bp insertion/deletion (I/D) polymorphism (rs28381975) and BC risk in an Iranian population. A total of 491 females, including 266 BC patients and 225 control subjects without cancer, were enrolled into the study. Our findings revealed that thePDCD6IP15 bp I/D polymorphism decreased the risk of BC in codominant (OR=0.44, 95%CI=0.31–0.65,p<0.0001, I/D versus DD;OR=0.39, 95%CI=0.17–0.88,p=0.030, I/I versus DD) and dominant (OR=0.44, 95%CI=0.30–0.63,p<0.0001, D/I + I/I versus D/D) tested inheritance models. Also, thePDCD6IPI allele significantly decreased the risk of BC (OR=0.59, 95%CI=0.45–0.78,p<0.001) compared to the D allele.

scholarly journals Ferroptosis and Cancer: Complex Relationship and Potential Application of Exosomes

2021 ◽  
Vol 9 ◽  
Author(s):  
Shuang Wu ◽  
Tianye Li ◽  
Weiwei Liu ◽  
Yongye Huang
Keyword(s):  
Cell Death ◽  
Cancer Treatment ◽  
Theoretical Basis ◽  
Genetic Basis ◽  
Epigenetic Modification ◽  
Lipid Hydroperoxides ◽  
Complex Relationship ◽  
Hallmarks Of Cancer ◽  
Cell Death Pathways ◽  
The Relationship

Cell death induction has become popular as a novel cancer treatment. Ferroptosis, a newly discovered form of cell death, features regulated, iron-dependent accumulation of lipid hydroperoxides. Since this word “ferroptosis” was coined, numerous studies have examined the complex relationship between ferroptosis and cancer. Here, starting from the intrinsic hallmarks of cancer and cell death, we discuss the theoretical basis of cell death induction as a cancer treatment. We review various aspects of the relationship between ferroptosis and cancer, including the genetic basis, epigenetic modification, cancer stem cells, and the tumor microenvironment, to provide information and support for further research on ferroptosis. We also note that exosomes can be applied in ferroptosis-based therapy. These extracellular vesicles can deliver different molecules to modulate cancer cells and cell death pathways. Using exosomes to control ferroptosis occurring in targeted cells is promising for cancer therapy.

scholarly journals Implication of Gut Microbiota in Cardiovascular Diseases

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Wenyi Zhou ◽  
Yiyu Cheng ◽  
Ping Zhu ◽  
M. I. Nasser ◽  
Xueyan Zhang ◽  
...  
Keyword(s):  
Cell Death ◽  
Cardiovascular Diseases ◽  
Programmed Cell Death ◽  
Gut Microbiota ◽  
Intestinal Flora ◽  
Short Chain Fatty Acids ◽  
Secondary Bile Acid ◽  
Cardiac Disorders ◽  
The Relationship

Emerging evidence has identified the association between gut microbiota and various diseases, including cardiovascular diseases (CVDs). Altered intestinal flora composition has been described in detail in CVDs, such as hypertension, atherosclerosis, myocardial infarction, heart failure, and arrhythmia. In contrast, the importance of fermentation metabolites, such as trimethylamine N-oxide (TMAO), short-chain fatty acids (SCFAs), and secondary bile acid (BA), has also been implicated in CVD development, prevention, treatment, and prognosis. The potential mechanisms are conventionally thought to involve immune regulation, host energy metabolism, and oxidative stress. However, numerous types of programmed cell death, including apoptosis, autophagy, pyroptosis, ferroptosis, and clockophagy, also serve as a key link in microbiome-host cross talk. In this review, we introduced and summarized the results from recent studies dealing with the relationship between gut microbiota and cardiac disorders, highlighting the role of programmed cell death. We hope to shed light on microbiota-targeted therapeutic strategies in CVD management.

scholarly journals New development of Immune checkpoints blockade in cancer immunotherapy

2019 ◽  
Vol 131 ◽  
pp. 01022
Author(s):  
Feixuan Wu
Keyword(s):  
Cell Death ◽  
Targeted Therapy ◽  
Programmed Cell Death ◽  
Cancer Treatment ◽  
Molecular Mechanisms ◽  
Nk Cell ◽  
Cytotoxic T Lymphocyte ◽  
Immune Checkpoints ◽  
Main Stream ◽  
Positive Effects

Immunotherapy has become the main stream in cancer treatment nowadays. It includes T cell, NK cell targeted therapy, as well as antibody targeted therapy and its derivatives. Recently immune checkpoints blockade (ICB) has been developed, which are said to be a better method in treatment. The release of negative regulators of immune activation has resulted in unprecedented rates of long-lasting tumor responses in patients with a variety of cancers. This can be achieved by antibodies blocking the cytotoxic T lymphocyte–associated protein 4 (CTLA-4), the programmed cell death 1 (PD-1) and programmed cell death ligand 1 (PDL-1) pathway or the lymphocyte-activated gene-3 (LAG-3) pathway, either alone or in combination. Improvement of treatment benefits from the research in molecular mechanisms of ICB. For example, mechanism of LAG-3 and its valid ligands is unclear, which leads to a misunderstanding that the antibody might be ineffective. After finding these results demonstrating that fibrinogen-like protein 1(FGL1) is an important functional ligand of LAG-3, it reveals the role of this LAG 3-FGL1 pathway in tumor immunity. Although there are some potential side effects, these therapies turn out to have lots of positive effects on most patients. Therefore, this review summarizes the latest advances, hoping that it may have a great contribution to the cancer treatment.

BH3-only proteins — evolutionarily conserved proapoptotic Bcl-2 family members essential for initiating programmed cell death

2002 ◽  
Vol 115 (8) ◽  
pp. 1567-1574 ◽  
Author(s):  
Philippe Bouillet ◽  
Andreas Strasser
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Family Members ◽  
Protein Family ◽  
Cell Stress ◽  
Protective Function ◽  
Evolutionarily Conserved ◽  
Apoptotic Cascade

The BH3-only members of the Bcl-2 protein family are essential initiators of programmed cell death and are required for apoptosis induced by cytotoxic stimuli. These proteins have evolved to recognise distinct forms of cell stress. In response, they unleash the apoptotic cascade by inactivating the protective function of the pro-survival members of the Bcl-2 family and by activating the Bax/Bax-like pro-apoptotic family members.

Sign in / Sign up

Export Citation Format

Share Document