scholarly journals Compound K Induces Apoptosis of Bladder Cancer T24 Cells Via Reactive Oxygen Species-Mediated p38 MAPK Pathway

2013 ◽  
Vol 28 (8) ◽  
pp. 607-614 ◽  
Author(s):  
Han Wang ◽  
Dandan Jiang ◽  
Jing Liu ◽  
Shuhong Ye ◽  
Shan Xiao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Bladder Cancer ◽  
P38 Mapk ◽  
Mapk Pathway ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Compound K ◽  
T24 Cells ◽  
P38 Mapk Pathway

scholarly journals Requirement of Reactive Oxygen Species-dependent Activation of ASK1-p38 MAPK Pathway for Extracellular ATP-induced Apoptosis in Macrophage

2008 ◽  
Vol 283 (12) ◽  
pp. 7657-7665 ◽  
Author(s):  
Takuya Noguchi ◽  
Ken Ishii ◽  
Hisashi Fukutomi ◽  
Isao Naguro ◽  
Atsushi Matsuzawa ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
P38 Mapk ◽  
Mapk Pathway ◽  
Reactive Oxygen ◽  
Extracellular Atp ◽  
Oxygen Species ◽  
P38 Mapk Pathway ◽  
Induced Apoptosis

Abstract 097: Recombinant Human Erythropoietin Prevents Reactive Oxygen Species - Induced Apoptosis Via Akt and p38 MAPK Pathway During Hypoxia/ Reperfusion Injury

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Asiya Parvin Allaudeen ◽  
Ajay Devendran ◽  
John E Baker ◽  
Anuradha Dhanasekaran
Keyword(s):  
Reactive Oxygen Species ◽  
P38 Mapk ◽  
Caspase 3 ◽  
Mapk Pathway ◽  
Intact Cell ◽  
Reactive Oxygen ◽  
Protective Role ◽  
Oxygen Species ◽  
Human Erythropoietin ◽  
In Cells

Erythropoietin (EPO) is a cytokine produced primarily in the kidney that is essential for red blood cell production. Apart from playing a role in hematopoiesis, EPO also has a protective role in heart myocytes, ovarian, glial cells brain and retinal diseases. In this study we observed that recombinant human EPO (rhEPO) reduces Hypoxia/ Reperfusion (H/R) injury by virtue of its effect on EPO receptor prosurvival signaling pathway, which ultimately leads to reduced expression of apoptotic proteins and increased survival of cardiomyocytes. H9C2 cells were exposed to H/R with or without pretreatment using 10, 15 and 20 U/ml of rhEPO. We determined viability using MTT, nuclear fragmentation by Hoechst staining, apoptotic nuclei by Acridine orange and Ethidium bromide, Reactive Oxygen Species (ROS) by Dicholorofluoresin Diacetate and activity of late apoptotic protease, Caspase-3 by colorimetric Caspase-3 assay. The expression of mitochondrial superoxide dismutase (MnSOD) by RT-PCR and Western blot, phospho-Akt and p38 MAPK by Confocal microscopy were analyzed. Cell viability is increased in cells pretreated with rhEPO compared to cell exposed to H/R. Cells subjected to H/R showed early apoptotic and late apoptotic cells but showed normal nuclei with intact cell membrane in cells pretreated with rhEPO. Intracellular production of ROS and Caspase-3 activity was decreased in cells pretreated with rhEPO compared to cells exposed to H/R. The expression of MnSOD RNA and protein was up-regulated in response to rhEPO, but not in H/R. The phosphorylative activation of Akt, p38MAPK progressively diminished during H/R but increased in rhEPO pretreated cells. We show that rhEPO prevents apoptosis in cardiomyocytes, subjected to H/R injury via phosphorylation of Akt and p38MAPK. These results it is hoped would help us distinguish the cell signaling pathways involved in cardioprotection and thus would open new avenues in cardiovascular therapy.

scholarly journals Bladder Cancer Chemosensitivity Is Affected by Paraoxonase-2 Expression

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 175 ◽  
Author(s):  
Stefania Fumarola ◽  
Monia Cecati ◽  
Davide Sartini ◽  
Gianna Ferretti ◽  
Giulio Milanese ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Bladder Cancer ◽  
Caspase 3 ◽  
Reactive Oxygen ◽  
Caspase 8 ◽  
Activity Levels ◽  
Oxygen Species ◽  
T24 Cells ◽  
Before And After ◽  
And Migration

The goal of the current study was to identify potential roles of paraoxonase-2 in bladder carcinogenesis. T24 bladder cancer cells were transfected with plasmids inducing paraoxonase-2 silencing or overexpression. Upon the selection of clones stably down- or upregulating paraoxonase-2, cell proliferation, migration, and the production of reactive oxygen species were evaluated, before and after treatment with cisplatin and gemcitabine, used alone or in combination. The activity levels of both caspase-3 and caspase-8 were also analyzed. shRNA-mediated gene silencing and the overexpression of paraoxonase-2 revealed that the enzyme was able to promote both the proliferation and migration of T24 cells. Moreover, the knockdown of paraoxonase-2 was significantly associated with a reduced cell viability of T24 cells treated with chemotherapeutic drugs and led to both an increase of reactive oxygen species production and caspase-3 and caspase-8 activation. Conversely, under treatment with anti-neoplastic compounds, a higher proliferative capacity was found in T24 cells overexpressing paraoxonase-2 compared with controls. In addition, upon enzyme upregulation, both the production of reactive oxygen species and activation of caspase-3 and caspase-8 were reduced. Although further analyses will be required to fully understand the involvement of paraoxonase-2 in bladder tumorigenesis and in mechanisms leading to the development of chemoresistance, the data reported in this study seem to demonstrate that the enzyme could exert a great impact on tumor progression and susceptibility to chemotherapy, thus suggesting paraoxonase-2 as a novel and interesting molecular target for effective bladder cancer treatment.

Sign in / Sign up

Export Citation Format

Share Document