Autophagy in response to photodynamic therapy: cell survival vs. cell death

2009 ◽  
Author(s):  
Nancy L. Oleinick ◽  
Liang-yan Xue ◽  
Song-mao Chiu ◽  
Sheeba Joseph
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Cell Survival

Fluorous photosensitizers enhance photodynamic therapy with perfluorocarbon nanoemulsions

2017 ◽  
Author(s):  
Ellen Sletten ◽  
Rachael A. Day ◽  
Daniel A. Estabrook ◽  
Jessica K. Logan
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Induce Cell Death ◽  
Perfluorocarbon Nanoemulsions

<p>Photodynamic therapy (PDT) requires photosensitizer, light, and oxygen to induce cell death. The majority of efforts to advance PDT focus only on the first two components. Here, we employ perfluorocarbon nanoemulsions to simultaneously deliver oxygen and photosensitizer. We find that the implementation of fluorous soluble photosensitizers enhances the efficacy of PDT. </p>

Neuroglobin and Estrogen Receptors: A New Pathway of Cell Survival and Cell Death Balance

2015 ◽  
Vol 14 (2) ◽  
pp. 91-99 ◽  
Author(s):  
Maria T. Nuzzo ◽  
Marco Fiocchetti ◽  
Paolo Ascenzi ◽  
Maria Marino
Keyword(s):  
Cell Death ◽  
Estrogen Receptors ◽  
Cell Survival

scholarly journals LONP1 and ClpP cooperatively regulate mitochondrial proteostasis for cancer cell survival

Oncogenesis ◽  
2021 ◽  
Vol 10 (2) ◽  
Author(s):  
Yu Geon Lee ◽  
Hui Won Kim ◽  
Yeji Nam ◽  
Kyeong Jin Shin ◽  
Yu Jin Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Growth ◽  
Cell Survival ◽  
Cancer Cell ◽  
Stress Responses ◽  
Molecular Mechanisms ◽  
Tca Cycle ◽  
Mitochondrial Matrix ◽  
Mitochondrial Functions ◽  
Cancer Cell Survival

AbstractMitochondrial proteases are key components in mitochondrial stress responses that maintain proteostasis and mitochondrial integrity in harsh environmental conditions, which leads to the acquisition of aggressive phenotypes, including chemoresistance and metastasis. However, the molecular mechanisms and exact role of mitochondrial proteases in cancer remain largely unexplored. Here, we identified functional crosstalk between LONP1 and ClpP, which are two mitochondrial matrix proteases that cooperate to attenuate proteotoxic stress and protect mitochondrial functions for cancer cell survival. LONP1 and ClpP genes closely localized on chromosome 19 and were co-expressed at high levels in most human cancers. Depletion of both genes synergistically attenuated cancer cell growth and induced cell death due to impaired mitochondrial functions and increased oxidative stress. Using mitochondrial matrix proteomic analysis with an engineered peroxidase (APEX)-mediated proximity biotinylation method, we identified the specific target substrates of these proteases, which were crucial components of mitochondrial functions, including oxidative phosphorylation, the TCA cycle, and amino acid and lipid metabolism. Furthermore, we found that LONP1 and ClpP shared many substrates, including serine hydroxymethyltransferase 2 (SHMT2). Inhibition of both LONP1 and ClpP additively increased the amount of unfolded SHMT2 protein and enhanced sensitivity to SHMT2 inhibitor, resulting in significantly reduced cell growth and increased cell death under metabolic stress. Additionally, prostate cancer patients with higher LONP1 and ClpP expression exhibited poorer survival. These results suggest that interventions targeting the mitochondrial proteostasis network via LONP1 and ClpP could be potential therapeutic strategies for cancer.

scholarly journals A Screen for Mutations That Suppress the Phenotype of Drosophila armadillo, the β-Catenin Homolog

Genetics ◽  
2000 ◽  
Vol 155 (4) ◽  
pp. 1725-1740
Author(s):  
Rachel T Cox ◽  
Donald G McEwen ◽  
Denise L Myster ◽  
Robert J Duronio ◽  
Joseph Loureiro ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Adhesion ◽  
Programmed Cell Death ◽  
Cell Survival ◽  
Wnt Pathway ◽  
Genetic Modifier ◽  
Wnt Signaling Pathway ◽  
Adherens Junction ◽  
Cell Fates ◽  
Wnt Signal

Abstract During development signaling pathways coordinate cell fates and regulate the choice between cell survival or programmed cell death. The well-conserved Wingless/Wnt pathway is required for many developmental decisions in all animals. One transducer of the Wingless/Wnt signal is Armadillo/β-catenin. Drosophila Armadillo not only transduces Wingless signal, but also acts in cell-cell adhesion via its role in the epithelial adherens junction. While many components of both the Wingless/Wnt signaling pathway and adherens junctions are known, both processes are complex, suggesting that unknown components influence signaling and junctions. We carried out a genetic modifier screen to identify some of these components by screening for mutations that can suppress the armadillo mutant phenotype. We identified 12 regions of the genome that have this property. From these regions and from additional candidate genes tested we identified four genes that suppress arm: dTCF, puckered, head involution defective (hid), and Dpresenilin. We further investigated the interaction with hid, a known regulator of programmed cell death. Our data suggest that Wg signaling modulates Hid activity and that Hid regulates programmed cell death in a dose-sensitive fashion.

Combination of photodynamic therapy with doxorubicin in osteosarcoma: Cell death and the role of oxidative stress

2016 ◽  
Vol 61 ◽  
pp. S141
Author(s):  
B. Serambeque ◽  
G. Brites ◽  
M. Laranjo ◽  
G. Chohfi de Miguel ◽  
A. Serra ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Photodynamic Therapy ◽  
Osteosarcoma Cell

scholarly journals Steroid Hormone Control of Cell Death and Cell Survival: Molecular Insights Using RNAi

PLoS Genetics ◽  
2009 ◽  
Vol 5 (2) ◽  
pp. e1000379 ◽  
Author(s):  
Suganthi Chittaranjan ◽  
Melissa McConechy ◽  
Ying-Chen Claire Hou ◽  
J. Douglas Freeman ◽  
Lindsay DeVorkin ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Survival ◽  
Steroid Hormone ◽  
Hormone Control

scholarly journals Pancreatic islet cell survival following islet isolation: the role of cellular interactions in the pancreas

1999 ◽  
Vol 161 (3) ◽  
pp. 357-364 ◽  
Author(s):  
A Ilieva ◽  
S Yuan ◽  
RN Wang ◽  
D Agapitos ◽  
DJ Hill ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Survival ◽  
Islet Cell ◽  
Apoptotic Cell ◽  
Specific Cell ◽  
Cellular Interactions ◽  
Pancreatic Islet Cell ◽  
Beneficial Result ◽  
Trophic Effect ◽  
Ductal Epithelium

The purpose of this study was to characterize the trophic effect of pancreatic duct cells on the islets of Langerhans. Ductal epithelium and islets were isolated from hamster pancreata. In addition, duct-conditioned medium (DCM) was prepared from primary duct cultures that had been passaged twice to remove other cellular elements. Three experimental groups were then established: Group 1, 100 islets alone; Group 2, 100 islets+80 duct fragments; and Group 3, 100 islets in 25% DCM. All tissues were embedded in rat tail collagen for up to 12 days and the influence of pancreatic ductal epithelium on islet cell survival was examined. By day 12, 20.6+/-3. 0% (S.E.M.) of the islets cultured alone developed central necrosis, compared with 6.7+/-2.0% of the islets co-cultured with ducts and 5.6+/-1.5% of the islets cultured in DCM (P<0.05). The presence of apoptotic cell death was determined by a TdT-mediated dUTP-biotin nick end labelling (TUNEL) assay and by a specific cell death ELISA. DNA fragmentation in islets cultured alone was significantly increased compared with islets cultured either in the presence of duct epithelium or in DCM (P<0.05). More than 80% of TUNEL-positive cells were situated in the inner 80% of the islet area, suggesting that most were beta-cells. DCM was analysed for known growth factors. The presence of a large amount of IGF-II (34 ng/ml) and a much smaller quantity of nerve growth factor (4 ng/ml) was identified. When the apoptosis studies were repeated to compare islets alone, islets+DCM and islets+IGF-II, the cell death ELISA indicated that IGF-II produced the same beneficial result as DCM when compared with islets cultured alone. We conclude that pancreatic ductal epithelium promotes islet cell survival. This effect appears to be mediated in a paracrine manner by the release of IGF-II from cells in the ductal epithelium.

Photodynamic Therapy with Liposomal Zinc Phthalocyanine and Tirapazamine Increases Tumor Cell Death via DNA Damage

2017 ◽  
Vol 13 (2) ◽  
pp. 204-220 ◽  
Author(s):  
Mans Broekgaarden ◽  
Ruud Weijer ◽  
AlbertC. van Wijk ◽  
RuudC. Cox ◽  
MaartenR. Egmond ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Photodynamic Therapy ◽  
Tumor Cell ◽  
Zinc Phthalocyanine ◽  
Tumor Cell Death

scholarly journals Protection by Bcl-2 against apoptotic but not autophagic cell death after photodynamic therapy

Autophagy ◽  
2008 ◽  
Vol 4 (1) ◽  
pp. 125-127 ◽  
Author(s):  
Liang-yan Xue ◽  
Song-mao Chiu ◽  
Kashif Azizuddin ◽  
Sheeba Joseph ◽  
Nancy L. Oleinick
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Autophagic Cell Death
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