Different types of DNA cleavage involved in osteosarcoma cell death

1996 ◽  
Author(s):  
K Kanbe ◽  
H Watanabe
Keyword(s):  
Cell Death ◽  
Dna Cleavage ◽  
Osteosarcoma Cell ◽  
Different Types

scholarly journals The Crosstalk Between Long Non-Coding RNAs and Various Types of Death in Cancer Cells

2021 ◽  
Vol 20 ◽  
pp. 153303382110330
Author(s):  
Wenwen Tang ◽  
Shaomi Zhu ◽  
Xin Liang ◽  
Chi Liu ◽  
Linjiang Song
Keyword(s):  
Cell Death ◽  
Cancer Cell ◽  
Causes Of Death ◽  
Vital Role ◽  
Cancer Cell Proliferation ◽  
Biological Targets ◽  
Cancer Cell Death ◽  
Different Types ◽  
Non Coding Rnas ◽  
Tumor Death

With the increasing aging population, cancer has become one of the leading causes of death worldwide, and the number of cancer cases and deaths is only anticipated to grow further. Long non-coding RNAs (lncRNAs), which are closely associated with the expression level of downstream genes and various types of bioactivity, are regarded as one of the key regulators of cancer cell proliferation and death. Cell death, including apoptosis, necrosis, autophagy, pyroptosis, and ferroptosis, plays a vital role in the progression of cancer. A better understanding of the regulatory relationships between lncRNAs and these various types of cancer cell death is therefore urgently required. The occurrence and development of tumors can be controlled by increasing or decreasing the expression of lncRNAs, a method which confers broad prospects for cancer treatment. Therefore, it is urgent for us to understand the influence of lncRNAs on the development of different modes of tumor death, and to evaluate whether lncRNAs have the potential to be used as biological targets for inducing cell death and predicting prognosis and recurrence of chemotherapy. The purpose of this review is to provide an overview of the various forms of cancer cell death, including apoptosis, necrosis, autophagy, pyroptosis, and ferroptosis, and to describe the mechanisms of different types of cancer cell death that are regulated by lncRNAs in order to explore potential targets for cancer therapy.

Combination of photodynamic therapy with doxorubicin in osteosarcoma: Cell death and the role of oxidative stress

2016 ◽  
Vol 61 ◽  
pp. S141
Author(s):  
B. Serambeque ◽  
G. Brites ◽  
M. Laranjo ◽  
G. Chohfi de Miguel ◽  
A. Serra ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Photodynamic Therapy ◽  
Osteosarcoma Cell

scholarly journals Death Receptor-Induced Activation of Initiator Caspase 8 Is Antagonized by Serine/Threonine Kinase PAK4

2003 ◽  
Vol 23 (21) ◽  
pp. 7838-7848 ◽  
Author(s):  
Nerina Gnesutta ◽  
Audrey Minden
Keyword(s):  
Cell Death ◽  
Cell Survival ◽  
Intracellular Signaling ◽  
Death Receptor ◽  
Caspase 8 ◽  
Death Domain ◽  
Serine Threonine Kinase ◽  
Threonine Kinase ◽  
Different Types ◽  
Promote Cell Survival

ABSTRACT Normal cell growth requires a precisely controlled balance between cell death and survival. This involves activation of different types of intracellular signaling cascades within the cell. While some types of signaling proteins regulate apoptosis, or programmed cell death, other proteins within the cell can promote survival. The serine/threonine kinase PAK4 can protect cells from apoptosis in response to several different types of stimuli. As is the case for other members of the p21-activated kinase (PAK) family, one way that PAK4 may promote cell survival is by phosphorylating and thereby inhibiting the proapoptotic protein Bad. This leads in turn to the inhibition of effector caspases such as caspase 3. Here we show that in response to cytokines which activate death domain-containing receptors, such as the tumor necrosis factor and Fas receptors, PAK4 can inhibit the death signal by a different mechanism. Under these conditions, PAK4 inhibits apoptosis early in the caspase cascade, antagonizing the activation of initiator caspase 8. This inhibition, which does not require PAK4's kinase activity, may involve inhibition of caspase 8 recruitment to the death domain receptors. This role in regulating initiator caspases is an entirely novel role for the PAK proteins and suggests a new mechanism by which these proteins promote cell survival.

scholarly journals Internucleosomal DNA cleavage and neuronal cell survival/death

1993 ◽  
Vol 122 (3) ◽  
pp. 523-532 ◽  
Author(s):  
A Batistatou ◽  
LA Greene
Keyword(s):  
Cell Death ◽  
Cell Survival ◽  
Pc12 Cells ◽  
Dna Fragmentation ◽  
Cell Cultures ◽  
Pc12 Cell ◽  
Dna Cleavage ◽  
Sympathetic Neurons ◽  
Term Survival ◽  
Serum Withdrawal

Serum-free PC12 cell cultures have been used to study the mechanisms of neuronal death after neurotrophic factor deprivation. We previously reported that PC12 cells undergo "apoptotic" internucleosomal DNA cleavage after withdrawal of trophic support. Here, we have used a sensitive method to detect PC12 cell DNA fragmentation within three hrs of serum removal and have exploited this assay to examine several aspects regarding the mechanisms of neuronal survival/death. Major advantages of this assay are that it permits acute experiments to be performed well before other manifest signs of cell death and under conditions that cannot be applied chronically. We find that this apopotic DNA fragmentation is distinct from the random DNA degradation that occurs during necrotic death. Major observations include the following: (a) There is a good correlation between the ability of trophic substances to promote PC12 cell survival and to inhibit early DNA fragmentation. (b) Phorbol ester, an activator of PKC, acutely suppresses DNA fragmentation, but does not promote long-term survival or inhibition of endonuclease activity when applied chronically due to its downregulation of PKC. (c) Cells undergoing apoptosis within 3 h of serum withdrawal have a "commitment point" of only 1.0-1.5 h beyond which they can no longer be rescued by NGF. (d) Aurin, a non-carboxylic analog of the endonuclease inhibitor ATA, also inhibits DNA fragmentation and promotes short-term survival of PC12 cells. (e) Macromolecular synthesis is not required for DNA fragmentation or for NGF to prevent this event. (f) Extracellular Ca2+ is not required for internucleosomal DNA cleavage caused by serum withdrawal or for suppression of this by NGF. (g) DNA fragmentation can also be detected in cultures of rat sympathetic neurons as early as 10 h after removal of NGF. As in PC12 cell cultures, this precedes morphological signs of cell death.

Mechanisms of death induced by cisplatin in proximal tubular epithelial cells: apoptosis vs. necrosis

1996 ◽  
Vol 270 (4) ◽  
pp. F700-F708 ◽  
Author(s):  
W. Lieberthal ◽  
V. Triaca ◽  
J. Levine
Keyword(s):  
Cell Death ◽  
Dna Cleavage ◽  
Primary Cultures ◽  
Cell Monolayer ◽  
Membrane Integrity ◽  
Ladder Pattern ◽  
Proximal Tubular Epithelial Cells ◽  
Proximal Tubular ◽  
High Concentrations ◽  
Induced Apoptosis

We have examined the mechanisms of cell death induced by cisplatin in primary cultures of mouse proximal tubular cells. High concentrations of cisplatin (800 microM) led to necrotic cell death over a few hours. Much lower concentrations of cisplatin (8 microM) led to apoptosis, which caused loss of the cell monolayer over several days. Necrosis was characterized by a cytosolic swelling and early loss of plasma membrane integrity. In contrast, early features of cells undergoing apoptosis included cell shrinkage and loss of attachment to the monolayers. Nuclear chromatin became condensed and fragmented in apoptosing cells. These features were absent in necrotic cells. DNA electrophoresis of cells exposed to 800 microM cisplatin yielded a "smear" pattern, due to random DNA degradation. In contrast, the DNA of apoptosing cells demonstrated a "ladder" pattern resulting from internucleosomal DNA cleavage. Antioxidants delayed cisplatin-induced apoptosis but not necrosis. Thus the mechanism of cell death induced by cisplatin is concentration dependent. Reactive oxygen species play a role in mediating apoptosis but not necrosis induced by cisplatin.

scholarly journals Cross Talk Between Autophagy and Apoptosis Contributes to ZnO Nanoparticle-Induced Human Osteosarcoma Cell Death

2018 ◽  
Vol 7 (17) ◽  
pp. 1800332 ◽  
Author(s):  
Guanping He ◽  
Yunlong Ma ◽  
Ye Zhu ◽  
Lei Yong ◽  
Xiao Liu ◽  
...  
Keyword(s):  
Cell Death ◽  
Cross Talk ◽  
Osteosarcoma Cell ◽  
Zno Nanoparticle ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cell

scholarly journals Indirubin and Indirubin Derivatives for Counteracting Proliferative Diseases

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Tina Blažević ◽  
Elke H. Heiss ◽  
Atanas G. Atanasov ◽  
Johannes M. Breuss ◽  
Verena M. Dirsch ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Active Component ◽  
Clinical Results ◽  
Chronic Myelocytic Leukemia ◽  
Myelocytic Leukemia ◽  
Pharmacokinetic Properties ◽  
Different Types ◽  
Traditional Chinese Medicine Formulation ◽  
Made In

Indirubin is the active component of Danggui Longhui Wan, a traditional Chinese medicine formulation. The encouraging clinical results from the 1980s obtained in chronic myelocytic leukemia patients treated with indirubin stimulated numerous studies on this compound. These investigations explored the use of indirubin in different types of cancer and reported the synthesis of novel derivatives with improved chemical and pharmacokinetic properties. In this paper, we review the impressive progress that has been made in elucidating the mechanistic understanding of how indirubin and its derivatives affect physiological and pathophysiological processes, mainly by inhibition of cell proliferation and induction of cell death. Furthermore, we survey the therapeutic use of these compounds in combating proliferative diseases such as cancer, restenosis, and psoriasis.

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