scholarly journals Differences of Key Proteins between Apoptosis and Necroptosis

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Min Yeong Park ◽  
Sang Eun Ha ◽  
Preethi Vetrivel ◽  
Hun Hwan Kim ◽  
Pritam Bhangwan Bhosale ◽  
...  

Many different types of programmed cell death (PCD) have been identified, including apoptosis and necroptosis. Apoptosis is a type of cell death that is controlled by various genes. It is in charge of eliminating aberrant cells such as cancer cells, replenishing normal cells, and molding the body as it develops. Necroptosis is a type of programmed cell death that combines necrosis and apoptosis. In other words, it takes on a necrotic appearance, although cells die in a controlled manner. Various investigations of these two pathways have revealed that caspase-8, receptor-interacting serine/threonine-protein kinase 1 (RIPK1), and RIPK3 are crucial proteins in charge of the switching between these two pathways, resulting in the activation or inhibition of necroptosis. In this review, we have summarized the key proteins between apoptosis and necroptosis.

2018 ◽  
Vol 1 (1) ◽  
pp. 12-23
Author(s):  
Diego Fernández-Lázaro ◽  
◽  
César Ignacio Fernández-Lázaro ◽  
Martínez Alfredo Córdova ◽  
◽  
...  

Programmed cell death is an essential physiological and biological process for the proper development and functioning of the organism. Apoptosis is the term that describes the most frequent form of programmed cell death and derives from the morphological characteristics of this type of death caused by cellular suicide. Apoptosis is highly regulated to maintain homeostasis in the body, since its imbalances by increasing and decreasing lead to different types of diseases. In this review, we aim to describe the mechanisms of cell death and the pathways through apoptosis is initiated, transmitted, regulated, and executed.


Cancers ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 1563 ◽  
Author(s):  
Nethaji Muniraj ◽  
Sumit Siddharth ◽  
Dipali Sharma

Each cell in our body is designed with a self-destructive trigger, and if damaged, can happily sacrifice itself for the sake of the body. This process of self-destruction to safeguard the adjacent normal cells is known as programmed cell death or apoptosis. Cancer cells outsmart normal cells and evade apoptosis and it is one of the major hallmarks of cancer. The cardinal quest for anti-cancer drug discovery (bioactive or synthetic compounds) is to be able to re-induce the so called “programmed cell death” in cancer cells. The importance of bioactive compounds as the linchpin of cancer therapeutics is well known as many effective chemotherapeutic drugs such as vincristine, vinblastine, doxorubicin, etoposide and paclitaxel have natural product origins. The present review discusses various bioactive compounds with known anticancer potential, underlying mechanisms by which they induce cell death and their preclinical/clinical development. Most bioactive compounds can concurrently target multiple signaling pathways that are important for cancer cell survival while sparing normal cells hence they can potentially be the silver bullets for targeting cancer growth and metastatic progression.


2016 ◽  
Vol 5 (5) ◽  
Author(s):  
Joe Antony Jacob ◽  
Jumah Masoud Mohammad Salmani ◽  
Baoan Chen

AbstractMagnetic nanoparticles are renowned for their anticancer activity. Recent studies have elucidated that magnetic nanoparticles induce cytotoxicity by induction of apoptosis in cancer cells. The magnetic nanoparticles can also be biosynthesized, and this presents an added advantage along with the concept of limited toxicity to normal cells. This review focuses on the mechanistic studies performed on the anticancer activity of different types of magnetic nanoparticles. Apoptosis was shown to be the most plausible reason behind the cell death mediated by various types of magnetic nanoparticles.


Blood ◽  
1993 ◽  
Vol 82 (1) ◽  
pp. 15-21 ◽  
Author(s):  
L Sachs ◽  
J Lotem

Programmed cell death (apoptosis) is a normal process by which cells are eliminated during normal embryonic development and in adult life. Disruption of this normal process resulting in illegitimate cell survival can cause developmental abnormalities and facilitate cancer development. Normal cells require certain viability factors and undergo programmed cell death when these factors are withdrawn. The viability factors are required throughout the differentiation process from immature to mature cells. Although many viability factors are also growth factors, viability and growth are separately regulated. Viability factors can have clinical value in decreasing the loss of normal cells including the loss that occurs after irradiation, exposure to other cytotoxic agents or virus infection including AIDS. There is no evidence that occurs after irradiation, exposure to other cytotoxic agents or virus infection including AIDS. There is no evidence that cancer cells are immortal. Programmed cell death can be induced in leukemic cells by removal of viability factors, by cytotoxic therapeutic agents, or by the tumor-suppressor gene wild-type p53. All these forms of induction of programmed cell death in leukemic cells can be suppressed by the same viability factors that suppress programmed cell death in normal cells. A tumor-promoting phorbol ester can also suppress this death program. The induction of programmed cell death can be enhanced by deregulated expression of the gene c-myc and suppressed by the gene bcl-2. Mutant p53 and bcl-2 suppress the enhancing effect on cell death of deregulated c-myc, and thus allow induction of cell proliferation and inhibition of differentiation which are other functions of deregulated c-myc. The suppression of cell death by mutant p53 and bcl-2 increases the probability of developing cancer. The suppression of programmed cell death in cancer cells by viability factors suggests that decreasing the level of these factors may increase the effectiveness of cytotoxic cancer therapy. Treatments that downregulate the expression or activity of mutant p53 and bcl-2 in cancer cells should also be useful for therapy.


2015 ◽  
Vol 8 (2) ◽  
Author(s):  
Tarek Omaiche

De nos jours, le traitement le plus répandu contre les cancers est la chimiothérapie. C'est une pratique qui se résume à l’utilisation des médicaments qui tuent les cellules qui se divisent rapidement. Cependant, la chimiothérapie est inefficace pour le traitement de certains cancers comme la leucémie aigüe myéloblastique(LMA).Ce type du cancer affecte les cellules souches responsables de la production des plaquettes, des globules rouges et blancs. Cette approche est souvent trop intense puisqu’elle tue  les normales cellulaires qui sont important pour la fonction du corps. Dans ce contexte, le professeur Paul Spagnuolo et son équipe à l’Université de Waterloo ont récemment reporté l’existence d’un lipide de l’avocat nommé l’avocatin B, qui peut efficacement tuer les cellules souches cancéreuses leucémiques sans endommager les cellules souches normales. L’avocatin B affecte l’oxydation des acides gras et réduit la production de l’NADPH, l’NAD et le GSH, des molécules essentielles pour le contrôle du stress oxydatif cellulaire. [1] En absence des défenses anti-oxydantes, les cellules cancéreuses succombent à la mort cellulaire programmée (apoptose).Now a days the most common treatment against cancer is chemotheraphy.This is a practise which uses medications who kills rapidly diving cells.Chemotheraphy is an ineffective treatment against certain cancers like acute myelodi leukemia(AML).This type of cancer affects the stem cells respondisble for the production of platelets,red and white blood cells.This approach is often to much/intense since it kills normal cells which are mportnat for the function of the body.In this context,Dr.Paul Spagnulo and his team at the University of Waterloo have recently reported dthe existence of a lipid in avacodo's called avocatin B,which  can effectively kill the cancer cells without damaging the normal cells.Avocatin B affects the oxidation of fatty acids and reduces(?) the production of NADPH, NAD and GSH; molecules that are essential for the control of oxidative stress. [1] These factors eventually lead to a programmed cell death (apoptosis).        


Impact ◽  
2020 ◽  
Vol 2020 (7) ◽  
pp. 37-39
Author(s):  
Masao Suzuki

The cells responsible for cancer start their journey much like any other in the body. However, they grow uncontrollably through the body as a result of the accumulation of certain mutations. If left unchecked, cancer will impact on a number of the human body's key processes, leading, ultimately, to death. There are many challenges associated with treating this disease, but they generally stem from the difficulty in differentiating the disease from the host and the ability of even a few cells to survive, recover and return. The most common treatments generally combine surgery with some type of chemotherapy or radiotherapy. Chemotherapy utilises chemicals that kill fast-growing cells and thereby disproportionally affect the rapidly multiplying cancer cells. Radiotherapy targets the tumour with radiation to cause damage and cell death. Both have their advantages and disadvantages, and both are often not 100 per cent effective. To improve these treatments, it is necessary to understand more about their precise effects on cells and, particularly, what defences cells have against their effects. Senior Principal Researcher Dr Masao Suzuki of the National Institutes for Quantum and Radiological Science and Technology (QST) is utilising the considerable radiological resources of QST to investigate the effects of different types of radiation on cells under different conditions.


Impact ◽  
2021 ◽  
Vol 2021 (6) ◽  
pp. 21-23
Author(s):  
Masao Suzuki

The cells responsible for cancer start their journey much like any other in the body. However, they grow uncontrollably through the body as a result of the accumulation of certain mutations. If left unchecked, cancer will impact on a number of the human body's key processes, leading, ultimately, to death. There are many challenges associated with treating this disease, but they generally stem from the difficulty in differentiating the disease from the host and the ability of even a few cells to survive, recover and return. The most common treatments generally combine surgery with some type of chemotherapy or radiotherapy. Chemotherapy utilises chemicals that kill fast-growing cells and thereby disproportionally affect the rapidly multiplying cancer cells. Radiotherapy targets the tumour with radiation to cause damage and cell death. Both have their advantages and disadvantages, and both are often not 100 per cent effective. To improve these treatments, it is necessary to understand more about their precise effects on cells and, particularly, what defences cells have against their effects. Senior Principal Researcher Dr Masao Suzuki of the National Institutes for Quantum and Radiological Science and Technology (QST) is utilising the considerable radiological resources of QST to investigate the effects of different types of radiation on cells under different conditions.


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