CELL DIFFERENTIATION IS ASSOCIATED TO DMSO-INDUCED PROGRAMMED CELL DEATH

1996 ◽  
Vol 24 (4) ◽  
pp. 555S-555S
Author(s):  
Oriana Trubiani ◽  
Marina Ciancarelli ◽  
Roberto Di Primio
2018 ◽  
Author(s):  
Dustin Lane

Programmed cell death signaling networks are frequently activated to coordinate the process of cell differentiation, and a variety of apoptotic events can mediate the process. This can include the ligation of death receptors, the activation of downstream caspases, and the induction of chromatin fragmentation, and all of these events can occur without downstream induction of death. Importantly, regulators of programmed cell death also have established roles in mediating differentiation. This review will provide an overview of apoptosis and its regulation by Inhibitors of Apoptosis (IAPs) and Bcl-2 family members. It will then outline the cross-talk between NF-ĸB and apoptotic signaling in the regulation of apoptosis before discussing the function of these regulators in the control of cell differentiation. It will end on a discussion of how a DNA damage-directed, cell cycle-dependent differentiation program may be controlled across multiple passages through cell cycle, and will assert that the failure to properly differentiate is the underlying cause of cancer.


2018 ◽  
Author(s):  
Dustin Lane

Programmed cell death signaling networks are frequently activated to coordinate the process of cell differentiation, and a variety of apoptotic events can mediate the process. This can include the ligation of death receptors, the activation of downstream caspases, and the induction of chromatin fragmentation, and all of these events can occur without downstream induction of death. Importantly, regulators of programmed cell death also have established roles in mediating differentiation. This review will provide an overview of apoptosis and its regulation by Inhibitors of Apoptosis (IAPs) and Bcl-2 family members. It will then outline the cross-talk between NF-ĸB and apoptotic signaling in the regulation of apoptosis before discussing the function of these regulators in the control of cell differentiation. It will end on a discussion of how a DNA damage-directed, cell cycle-dependent differentiation program may be controlled across multiple passages through cell cycle, and will assert that the failure to properly differentiate is the underlying cause of cancer.


Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1017
Author(s):  
Chun-Seob Ahn ◽  
Jeong-Geun Kim ◽  
Insug Kang ◽  
Yoon Kong

The small liver fluke Clonorchis sinensis causes hepatobiliary ductal infections in humans. Clonorchiasis is characterized histopathologically by ductal dysplasia, hyperplasia and metaplasia, which closely resembles cholangiocarcinoma (CCA). The disruption of programmed cell death is critical for malignant transformation, while molecular events underlying these phenomena have poorly been understood in clonorchiasis-related CCA tumorigenesis. We incorporated recombinant C. sinensis omega-class glutathione transferase (rCsGSTo) 1 or 2 into human intrahepatic biliary epithelial cells (HIBECs) and analyzed pathophysiological alterations of HIBECs upon the application of oxidative stress. rCsGSTos partially but significantly rescued HIBECs from cell death by inhibiting oxidative stress-induced apoptosis (p < 0.01). rCsGSTos modulated transcriptional levels of numerous genes. We analyzed 13 genes involved in programmed cell death (the upregulation of five antiapoptotic and two apoptotic genes, and the downregulation of one antiapoptotic and five apoptotic genes) and 11 genes associated with cell differentiation (the increase in seven and decrease in four genes) that showed significant modifications (p < 0.05). The induction profiles of the mRNA and proteins of these differentially regulated genes correlated well with each other, and mostly favored apoptotic suppression and/or cell differentiation. We detected increased active, phosphorylated forms of Src, PI3K/Akt, NF-κB p65, MKK3/6 and p38 MAPK, but not JNK and ERK1/2. CsGSTos were localized in the C. sinensis-infected rat cholangiocytes, where cytokeratin 19 was distributed. Our results demonstrated that CsGSTos excreted to the biliary lumen are internalized and accumulated in the host cholangiocytes. When cholangiocytes underwent oxidative stressful condition, CsGSTos appeared to be critically involved in both antiapoptotic process and the differentiation of host cholangiocytes through the regulation of target genes following the activation of responsible signal molecules.


1997 ◽  
Vol 137 (5) ◽  
pp. 714-720 ◽  
Author(s):  
A. FAYYAZI ◽  
A. SORURI ◽  
H.J. RADZUN ◽  
J.H. PETERS ◽  
H. BERGER

1997 ◽  
Vol 137 (5) ◽  
pp. 714-720 ◽  
Author(s):  
A. FAYYAZI ◽  
A. SORURI ◽  
H.J. RADZUN ◽  
J.H. PETERS ◽  
H. BERGER

IUBMB Life ◽  
2011 ◽  
Vol 63 (10) ◽  
pp. 922-929 ◽  
Author(s):  
Jesús Chimal-Monroy ◽  
René Fernando Abarca-Buis ◽  
Rodrigo Cuervo ◽  
Martha Díaz-Hernández ◽  
Marcia Bustamante ◽  
...  

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