Caspase-independent cell death?

RA Lockshin, Z Zakeri - Oncogene, 2004 - nature.com
Many cells die with apoptotic morphology and with documented activation of an effector
caspase, but there are also many exceptions. Cells frequently display activation of other …

Exercise preconditioning reduces neuronal apoptosis in stroke by up-regulating heat shock protein-70 (heat shock protein-72) and extracellular-signal-regulated …

B Liebelt, P Papapetrou, A Ali, M Guo, X Ji, C Peng… - Neuroscience, 2010 - Elsevier
Exercise preconditioning induces neuroprotection after stroke. We investigated the
beneficial role of heat shock protein-70 (HSP-70) and phosphorylated extracellular-signal …

[HTML][HTML] Combined inhibition of MAPK and mTOR signaling inhibits growth, induces cell death, and abrogates invasive growth of melanoma cells

KG Lasithiotakis, TW Sinnberg, B Schittek… - Journal of Investigative …, 2008 - Elsevier
The RAS–RAF–MEK–ERK and PI3K–AKT–mTOR signaling pathways are activated through
multiple mechanisms and appear to play a major role in melanoma progression. Herein, we …

Vorinostat and sorafenib synergistically kill tumor cells via FLIP suppression and CD95 activation

G Zhang, MA Park, C Mitchell, H Hamed… - Clinical cancer …, 2008 - AACR
Abstract Purpose and Design: Mechanism (s) by which the multikinase inhibitor sorafenib
and the histone deacetylase inhibitor vorinostat interact to kill hepatic, renal, and pancreatic …

The nonerythropoietic asialoerythropoietin protects against neonatal hypoxia‐ischemia as potently as erythropoietin

X Wang, C Zhu, X Wang, JG Gerwien… - Journal of …, 2004 - Wiley Online Library
Recently, erythropoietin (EPO) and the nonerythropoietic derivative asialoEPO have been
linked to tissue protection in the nervous system. In this study, we tested their effects in a …

Vorinostat and Sorafenib Increase CD95 Activation in Gastrointestinal Tumor Cells through a Ca2+-De novo Ceramide-PP2A-Reactive Oxygen Species–Dependent …

MA Park, C Mitchell, G Zhang, A Yacoub, J Allegood… - Cancer research, 2010 - AACR
The targeted therapeutics sorafenib and vorinostat interact in a synergistic fashion to kill
carcinoma cells by activating CD95, and this drug combination is entering phase I …

Homeostatic chemokines increase survival of B-chronic lymphocytic leukemia cells through inactivation of transcription factor FOXO3a

M Ticchioni, M Essafi, PY Jeandel, F Davi, JP Cassuto… - Oncogene, 2007 - nature.com
B-chronic lymphocytic leukemia (B-CLL) cell is characterized by the accumulation of long-
lived CD5+ B lymphocytes, whose survival in vivo is in part dependent on exogenous factors …

The role of erythropoietin and its receptor in growth, survival and therapeutic response of human tumor cells: from clinic to bench—a critical review

J Szenajch, G Wcislo, JY Jeong, C Szczylik… - … et Biophysica Acta (BBA …, 2010 - Elsevier
Recombinant human erythropoietin (rhEPO) has been used clinically to alleviate cancer-and
chemotherapy-related anemia. However, recent clinical trials have reported that rhEPO also …

Sorafenib and vorinostat kill colon cancer cells by CD95-dependent and-independent mechanisms

T Walker, C Mitchell, MA Park, A Yacoub, M Graf… - Molecular …, 2009 - ASPET
We examined the interaction between the multikinase inhibitor sorafenib and histone
deacetylase inhibitors. Sorafenib and vorinostat synergized (sorafenib+ vorinostat) to kill …

[HTML][HTML] Melatonin combined with endoplasmic reticulum stress induces cell death via the PI3K/Akt/mTOR pathway in B16F10 melanoma cells

HS Kim, TJ Kim, YM Yoo - PloS one, 2014 - journals.plos.org
This study investigated B16F10 melanoma cell death induced by melatonin combined with
endoplasmic reticulum (ER) stress through the PI3K/Akt/mTOR pathway. Cell viability was …