Expression of candidate cell death genes in cell lines during apoptosis

1994 ◽  
Vol 72 (11-12) ◽  
pp. 451-454 ◽  
Author(s):  
Georg Häcker ◽  
David L. Vaux
Keyword(s):  
Cell Death ◽  
Growth Factor ◽  
Interleukin 1Β ◽  
Mrna Levels ◽  
Converting Enzyme ◽  
Dependent Cell ◽  
Cell Death Gene ◽  
Low Levels ◽  
Cell Death Genes ◽  
Death Genes

We have cloned mouse candidate cell death genes RP-2 and nedd2 and used Northern blot analysis to study their expression in a growth-factor-dependent cell line (FDC-P1) that can be induced to undergo apoptosis by growth factor withdrawal and in a thymoma line (ST4) that undergoes apoptosis when irradiated. RP-2 was expressed in FDC-P1 cells even when not undergoing apoptosis, and mRNA levels did not increase when apoptosis was induced by growth factor withdrawal. FDC-P1 cells expressed two genes that are similar to the Caenorhabditis elegans cell death gene ced-3: a 3.7 kilobase (kb) nedd2 message and low levels of a 5-kb message for interleukin-1β converting enzyme. Levels of these messages did not change with the induction of cell death, but transfection of fibroblasts with constructs expressing nedd2 caused them to undergo apoptosis. These results suggest that expression of RP-2 and nedd2 is not sufficient for apoptosis, and if the products of these genes are involved in apoptosis of FDC-P1 cells, they are regulated by posttranslational mechanisms.Key words: apoptosis, RP-2, nedd2, interleukin-1β converting enzyme.

Interleukin-1α-converting enzyme (ICE) and related cell death genes ICErel-II and ICErel-III map to the same PAC clone at band 11q22.2-22.3

1997 ◽  
Vol 8 (8) ◽  
pp. 611-613 ◽  
Author(s):  
Jamal Nasir ◽  
Jane L. Theilmann ◽  
John P. Vaillancourt ◽  
Neil A. Munday ◽  
Ambereen Ali ◽  
...  
Keyword(s):  
Cell Death ◽  
Converting Enzyme ◽  
Related Cell ◽  
Interleukin 1Α ◽  
Cell Death Genes ◽  
Death Genes

scholarly journals Network Analysis Identifies Drug Targets and Small Molecules to Modulate Apoptosis Resistant Cancers

Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 851
Author(s):  
Samreen Fathima ◽  
Swati Sinha ◽  
Sainitin Donakonda
Keyword(s):  
Cell Death ◽  
Small Molecules ◽  
Drug Targets ◽  
Apoptotic Cell ◽  
Colon Adenocarcinoma ◽  
Interaction Networks ◽  
Small Cell Lung ◽  
Protein Protein Interaction ◽  
Cell Death Genes ◽  
Death Genes

Programed cell death or apoptosis fails to induce cell death in many recalcitrant cancers. Thus, there is an emerging need to activate the alternate cell death pathways in such cancers. In this study, we analyzed the apoptosis-resistant colon adenocarcinoma, glioblastoma multiforme, and small cell lung cancers transcriptome profiles. We extracted clusters of non-apoptotic cell death genes from each cancer to understand functional networks affected by these genes and their role in the induction of cell death when apoptosis fails. We identified transcription factors regulating cell death genes and protein–protein interaction networks to understand their role in regulating cell death mechanisms. Topological analysis of networks yielded FANCD2 (ferroptosis, negative regulator, down), NCOA4 (ferroptosis, up), IKBKB (alkaliptosis, down), and RHOA (entotic cell death, down) as potential drug targets in colon adenocarcinoma, glioblastoma multiforme, small cell lung cancer phenotypes respectively. We also assessed the miRNA association with the drug targets. We identified tumor growth-related interacting partners based on the pathway information of drug-target interaction networks. The protein–protein interaction binding site between the drug targets and their interacting proteins provided an opportunity to identify small molecules that can modulate the activity of functional cell death interactions in each cancer. Overall, our systematic screening of non-apoptotic cell death-related genes uncovered targets helpful for cancer therapy.

scholarly journals 1779 Cell Death Genes are Induced Immediately after Hypoxia-Reoxygenation (HR) in the Newborn Mouse Lung

2012 ◽  
Vol 97 (Suppl 2) ◽  
pp. A503-A503
Author(s):  
E. Wollen ◽  
A. Rognlien ◽  
M. Atneosen-Asegg ◽  
M. Wright ◽  
M. Bjoras ◽  
...  
Keyword(s):  
Cell Death ◽  
Mouse Lung ◽  
Newborn Mouse ◽  
Cell Death Genes ◽  
Death Genes ◽  
Hypoxia Reoxygenation

scholarly journals Phosphatidylinositol-3,4,5-Trisphosphate Is Required for Insulin-Like Growth Factor 1-Mediated Survival of 3T3-L1 Preadipocytes**This work was supported by a grant (to A.S.) from the Medical Research Council of Canada.

Endocrinology ◽  
2001 ◽  
Vol 142 (1) ◽  
pp. 205-212 ◽  
Author(s):  
AnneMarie Gagnon ◽  
Patti Dods ◽  
Nicolas Roustan-Delatour ◽  
Ching-Shih Chen ◽  
Alexander Sorisky
Keyword(s):  
Cell Death ◽  
Growth Factor ◽  
Mammalian Target Of Rapamycin ◽  
Inhibitory Effect ◽  
Tunel Staining ◽  
Insulin Like Growth Factor ◽  
Tissue Mass ◽  
Akt Phosphorylation ◽  
Dependent Cell ◽  
Phosphoinositide 3 Kinase

Abstract Adipocyte number, a determinant of adipose tissue mass, reflects the balance between the rates of proliferation/differentiation vs. apoptosis of preadipocytes. The percentage of 3T3-L1 preadipocytes undergoing cell death following serum deprivation was reduced by 10 nm insulin-like growth factor (IGF)-1 (from 50.0 ± 0.7% for control starved cells to 27.5 ± 3.1%). TUNEL staining confirmed the apoptotic nature of the cell death. The protective effect of IGF-1 was blocked by phosphoinositide 3-kinase (PI3K) inhibitors, wortmannin, and LY294002, but was unaffected by rapamycin, PD98059, or SB203580, which inhibit mammalian target of rapamycin (mTOR), ERK kinase (MEK1), and p38 MAPK respectively. Exogenous PI(3,4,5)P3 (10 μm), the principal product of IGF-1-stimulated PI3K in 3T3-L1 preadipocytes, had a modest survival effect on its own, reducing cell death from 47.9± 3.4% to 35.6 ± 3.5%. When added to the combination of IGF-1 and LY294002, PI(3,4,5)P3 reversed most of the inhibitory effect of LY294002 on IGF-1-dependent cell survival, protein kinase B/Akt phosphorylation, and caspase-3 activity. Taken together, these results implicate PI(3,4,5)P3 as a necessary signal for the anti-apoptotic action of IGF-1 on 3T3-L1 preadipocytes.

Sign in / Sign up

Export Citation Format

Share Document