scholarly journals Overexpression of Hematopoietically Expressed Homeoprotein Induces Nonapoptotic Cell Death in Mouse Prechondrogenic ATDC5 Cells

2011 ◽  
Vol 34 (10) ◽  
pp. 1589-1595
Author(s):  
Riyo Morimoto ◽  
Akiko Obinata
Keyword(s):  
Cell Death ◽  
Nonapoptotic Cell Death

Beyond apoptosis: nonapoptotic cell death in physiology and disease

2005 ◽  
Vol 83 (5) ◽  
pp. 579-588 ◽  
Author(s):  
Claudio A Hetz ◽  
Vicente Torres ◽  
Andrew F.G Quest
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Death Receptor ◽  
Receptor Signaling ◽  
Family Analysis ◽  
Caspase Family ◽  
Death Receptor Signaling ◽  
Apoptotic Pathways ◽  
Nonapoptotic Cell Death ◽  
High Degree

Apoptosis is a morphologically defined form of programmed cell death (PCD) that is mediated by the activation of members of the caspase family. Analysis of death-receptor signaling in lymphocytes has revealed that caspase-dependent signaling pathways are also linked to cell death by nonapoptotic mechanisms, indicating that apoptosis is not the only form of PCD. Under physiological and pathological conditions, cells demonstrate a high degree of flexibility in cell-death responses, as is reflected in the existence of a variety of mechanisms, including necrosis-like PCD, autophagy (or type II PCD), and accidental necrosis. In this review, we discuss recent data suggesting that canonical apoptotic pathways, including death-receptor signaling, control caspase-dependent and -independent cell-death pathways.Key words: apoptosis, necrosis, nonapoptotic programmed cell death, death receptors, ceramides.

scholarly journals Synthesis and Evaluation of Indole-Based Chalcones as Inducers of Methuosis, a Novel Type of Nonapoptotic Cell Death

2012 ◽  
Vol 55 (5) ◽  
pp. 1940-1956 ◽  
Author(s):  
Michael W. Robinson ◽  
Jean H. Overmeyer ◽  
Ashley M. Young ◽  
Paul W. Erhardt ◽  
William A. Maltese
Keyword(s):  
Cell Death ◽  
Nonapoptotic Cell Death

scholarly journals BNIP3 Is an RB/E2F Target Gene Required for Hypoxia-Induced Autophagy

2007 ◽  
Vol 27 (17) ◽  
pp. 6229-6242 ◽  
Author(s):  
Kristin Tracy ◽  
Benjamin C. Dibling ◽  
Benjamin T. Spike ◽  
James R. Knabb ◽  
Paul Schumacker ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Suppressor ◽  
Transcriptional Repression ◽  
Fetal Liver ◽  
Hypoxia Inducible Factor ◽  
Nutrient Deprivation ◽  
Primary Mouse ◽  
Direct Target ◽  
Nonapoptotic Cell Death

ABSTRACT Hypoxia and nutrient deprivation are environmental stresses governing the survival and adaptation of tumor cells in vivo. We have identified a novel role for the Rb tumor suppressor in protecting against nonapoptotic cell death in the developing mouse fetal liver, in primary mouse embryonic fibroblasts, and in tumor cell lines. Loss of pRb resulted in derepression of BNip3, a hypoxia-inducible member of the Bcl-2 superfamily of cell death regulators. We identified BNIP3 as a direct target of pRB/E2F-mediated transcriptional repression and showed that pRB attenuates the induction of BNIP3 by hypoxia-inducible factor to prevent autophagic cell death. BNIP3 was essential for hypoxia-induced autophagy, and its ability to promote autophagosome formation was enhanced under conditions of nutrient deprivation. Knockdown of BNIP3 reduced cell death, and remaining deaths were necrotic in nature. These studies identify BNIP3 as a key regulator of hypoxia-induced autophagy and suggest a novel role for the RB tumor suppressor in preventing nonapoptotic cell death by limiting the extent of BNIP3 induction in cells.

scholarly journals New Insight into the Effects of Metformin on Diabetic Retinopathy, Aging and Cancer: Nonapoptotic Cell Death, Immunosuppression, and Effects beyond the AMPK Pathway

2021 ◽  
Vol 22 (17) ◽  
pp. 9453
Author(s):  
Sheng-Kai Hsu ◽  
Kai-Chun Cheng ◽  
Miracle Oluebube Mgbeahuruike ◽  
Yi-Hsiung Lin ◽  
Chang-Yi Wu ◽  
...  
Keyword(s):  
Cell Death ◽  
Diabetic Retinopathy ◽  
Metabolic Stress ◽  
Glucose Deprivation ◽  
Ampk Pathway ◽  
Anticancer Effects ◽  
Pathway Activation ◽  
Nonapoptotic Cell Death ◽  
Amp Activated Protein Kinase

Under metabolic stress conditions such as hypoxia and glucose deprivation, an increase in the AMP:ATP ratio activates the AMP-activated protein kinase (AMPK) pathway, resulting in the modulation of cellular metabolism. Metformin, which is widely prescribed for type 2 diabetes mellitus (T2DM) patients, regulates blood sugar by inhibiting hepatic gluconeogenesis and promoting insulin sensitivity to facilitate glucose uptake by cells. At the molecular level, the most well-known mechanism of metformin-mediated cytoprotection is AMPK pathway activation, which modulates metabolism and protects cells from degradation or pathogenic changes, such as those related to aging and diabetic retinopathy (DR). Recently, it has been revealed that metformin acts via AMPK- and non-AMPK-mediated pathways to exert effects beyond those related to diabetes treatment that might prevent aging and ameliorate DR. This review focuses on new insights into the anticancer effects of metformin and its potential modulation of several novel types of nonapoptotic cell death, including ferroptosis, pyroptosis, and necroptosis. In addition, the antimetastatic and immunosuppressive effects of metformin and its hypothesized mechanism are also discussed, highlighting promising cancer prevention strategies for the future.

Sign in / Sign up

Export Citation Format

Share Document