Faculty Opinions recommendation of Inhibition of neuroepithelial patched-induced apoptosis by sonic hedgehog.

2003 ◽  
Author(s):  
Kermit Carraway
Keyword(s):  
Sonic Hedgehog ◽  
Induced Apoptosis

672: Regulation of Cavernous Nerve Injury-Induced Apoptosis by Sonic Hedgehog

2007 ◽  
Vol 177 (4S) ◽  
pp. 225-225
Author(s):  
Carol A. Podlasek ◽  
Yi Tang ◽  
Cynthia L. Meraz ◽  
Kevin E. McKenna ◽  
Kevin T. McVary
Keyword(s):  
Nerve Injury ◽  
Sonic Hedgehog ◽  
Cavernous Nerve ◽  
Induced Apoptosis ◽  
Cavernous Nerve Injury

Guggulsterone sensitizes glioblastoma cells to Sonic hedgehog inhibitor SANT-1 induced apoptosis in a Ras/NFκB dependent manner

2013 ◽  
Vol 336 (2) ◽  
pp. 347-358 ◽  
Author(s):  
Deobrat Dixit ◽  
Ruchi Ghildiyal ◽  
Nikhil Ponnor Anto ◽  
Sourav Ghosh ◽  
Vivek Sharma ◽  
...  
Keyword(s):  
Sonic Hedgehog ◽  
Dependent Manner ◽  
Glioblastoma Cells ◽  
Induced Apoptosis ◽  
Hedgehog Inhibitor

scholarly journals Inhibition of the sonic hedgehog pathway activates TGF-β-activated kinase (TAK1) to induce autophagy and suppress apoptosis in thyroid tumor cells

2021 ◽  
Vol 12 (5) ◽  
Author(s):  
Sumei Li ◽  
Jingxiang Wang ◽  
Yurong Lu ◽  
Yuqing Zhao ◽  
Richard A. Prinz ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Sonic Hedgehog ◽  
Anaplastic Thyroid Cancer ◽  
Thyroid Tumor ◽  
Shh Pathway ◽  
Compound C ◽  
Mechanistic Investigation ◽  
Pathway Inhibition ◽  
Induced Apoptosis ◽  
Thyroid Cancer Cell Lines

AbstractThe sonic hedgehog (Shh) pathway is highly activated in a variety of malignancies and plays important roles in tumorigenesis, tumor growth, drug resistance, and metastasis. Our recent study showed that the inhibitors of the Shh pathway such as cyclopamine (CP), a Smothened (SMO) inhibitor, and GANT61, a Gli1 inhibitor, have modest inhibitory effects on thyroid tumor cell proliferation and tumor growth. The objective of this study was to determine whether autophagy was induced by inhibition of the Shh pathway and could negatively regulate GANT61-induced apoptosis. Here we report that inhibition of the Shh pathway by Gli1 siRNA or by cyclopamine and GANT61 induced autophagy in SW1736 and KAT-18 cells, two anaplastic thyroid cancer cell lines; whereas Gli1 overexpression suppressed autophagy. Mechanistic investigation revealed that inhibition of the Shh pathway activated TAK1 and its two downstream kinases, the c-Jun-terminal kinase (JNK) and AMP-activated protein kinase (AMPK). GANT61-induced autophagy was blocked by TAK1 siRNA and the inhibitors of TAK1 (5Z-7-oxozeaenol, 5Z), JNK (SP600125), and AMPK (Compound C, CC). Inhibition of autophagy by chloroquine and 5Z and by TAK1 and Beclin-1 siRNA enhanced GANT61-induced apoptosis and its antiproliferative activity. Our study has shown that inhibition of the Shh pathway induces autophagy by activating TAK1, whereas autophagy in turn suppresses GANT61-induced apoptosis. We have uncovered a previously unrecognized role of TAK1 in Shh pathway inhibition-induced autophagy and apoptosis.

scholarly journals Lycium barbarumPolysaccharides Protect against Trimethyltin Chloride-Induced Apoptosis via Sonic Hedgehog and PI3K/Akt Signaling Pathways in Mouse Neuro-2a Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-18 ◽  
Author(s):  
Wanyun Zhao ◽  
Xiaoqi Pan ◽  
Tao Li ◽  
Changchun Zhang ◽  
Nian Shi
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathways ◽  
Sonic Hedgehog ◽  
Glycogen Synthase ◽  
Akt Signaling ◽  
Dependent Manner ◽  
Lycium Barbarum ◽  
N2a Cells ◽  
Trimethyltin Chloride ◽  
Induced Apoptosis

Trimethyltin chloride (TMT) is a classic neurotoxicant that can cause severe neurodegenerative diseases. Some signaling pathways involving cell death play pivotal roles in the central nervous system. In this study, the role of Sonic Hedgehog (Shh) and PI3K/Akt pathways in TMT-induced apoptosis and protective effect ofLycium barbarumpolysaccharides (LBP) on mouse neuro-2a (N2a) cells were investigated. Results showed that TMT treatment significantly enhanced apoptosis, upregulated proapoptotic Bax, downregulated antiapoptotic Bcl-2 expression, and increased caspase-3 activity in a dose-dependent manner in N2a cells. TMT induced oxidative stress in cells, performing reactive oxygen species (ROS) and malondialdehyde (MDA) excessive generation, and superoxide dismutase (SOD) activity reduction. TMT significantly decreased phosphorylated glycogen synthase kinase-3β(GSK-3β) and inhibited Shh and PI3K/Akt pathways. However, the addition of LBP upregulated GSK-3βphosphorylation, activated Shh and PI3K/Akt pathways, and eventually reduced apoptosis and oxidative stress caused by TMT. The interaction between Shh and PI3K/Akt pathways was clarified by specific PI3K inhibitor LY294002 or Shh inhibitor GDC-0449. Moreover, LY294002 and GDC-0449 pretreatment both induced phosphorylated GSK-3βdownregulation and significantly promoted apoptosis induced by TMT. These results suggest that LBP could reduce TMT-induced N2a cells apoptosis by regulating GSK-3βphosphorylation, Shh, and PI3K/Akt signaling pathways.

Absence of temporal ordering of apoptotic features in heat-shock treated leukemia and lymphoma cell lines

1996 ◽  
Vol 54 ◽  
pp. 758-759
Author(s):  
D. W. Fairbain ◽  
M.D. Standing ◽  
K.L. O'Neill
Keyword(s):  
Heat Shock ◽  
Cell Lines ◽  
Chromatin Condensation ◽  
Membrane Integrity ◽  
Resistant Cell ◽  
Membrane Blebbing ◽  
Late Loss ◽  
Induced Apoptosis ◽  
Dying Cells ◽  
In Cells

Apoptosis is a genetically defined response to physiological stimuli that results in cellular suicide. Features common to apoptotic cells include chromatin condensation, oligonucleosomal DNA fragmentation, membrane blebbing, nuclear destruction, and late loss of ability to exclude vital dyes. These characteristics contrast markedly from pathological necrosis, in which membrane integrity loss is demonstrated early, and other features of apoptosis, which allow a non-inflammatory removal of dead and dying cells, are absent. Using heat shock-induced apoptosis as a model for examining stress response in cells, we undertook to categorize a variety of human leukemias and lymphomas with regard to their response to heat shock. We were also interested in determining whether a common temporal order was followed in cells dying by apoptosis. In addition, based on our previous results, we investigated whether increasing heat load resulted in increased apoptosis, with particular interest in relatively resistant cell lines, or whether the mode of death changed from apoptosis to necrosis.

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