The role of cyclooxygenase enzymes in the growth of human gall bladder cancer cells

2000 ◽  
Vol 21 (7) ◽  
pp. 1403-1409 ◽  
Author(s):  
Erik M. Grossman ◽  
Walter E. Longo ◽  
Ninder Panesar ◽  
John E. Mazuski ◽  
Donald L. Kaminski
2000 ◽  
Vol 21 (7) ◽  
pp. 1403-1409 ◽  
Author(s):  
Erik M. Grossman ◽  
Walter E. Longo ◽  
Ninder Panesar ◽  
John E. Mazuski ◽  
Donald L. Kaminski

2019 ◽  
Vol 19 (6) ◽  
pp. 826-837 ◽  
Author(s):  
Pratibha Pandey ◽  
Preeti Bajpai ◽  
Mohammad H. Siddiqui ◽  
Uzma Sayyed ◽  
Rohit Tiwari ◽  
...  

Background:Plant sterols have proven a potent anti-proliferative and apoptosis inducing agent against several carcinomas including breast and prostate cancers. Jab1 has been reported to be involved in the progression of numerous carcinomas. However, antiproliferative effects of sterols against Jab1 in gall bladder cancer have not been explored yet.Objective:In the current study, we elucidated the mechanism of action of stigmasterol regarding apoptosis induction mediated via downregulation of Jab1 protein in human gall bladder cancer cells.Methods:In our study, we performed MTT and Trypan blue assay to assess the effect of stigmasterol on cell proliferation. In addition, RT-PCR and western blotting were performed to identify the effect of stigmasterol on Jab1 and p27 expression in human gall bladder cancer cells. We further performed cell cycle, Caspase-3, Hoechst and FITC-Annexin V analysis, to confirm the apoptosis induction in stigmasterol treated human gall bladder cancer cells.Results:Our results clearly indicated that stigmasterol has up-regulated the p27 expression and down-regulated Jab1 gene. These modulations of genes might occur via mitochondrial apoptosis signaling pathway. Caspase-3 gets activated with the apoptotic induction. Increase in apoptotic cells and DNA were confirmed through annexin V staining, Hoechst staining, and cell cycle analysis.Conclusion:Thus, these results strongly suggest that stigmasterol has the potential to be considered as an anticancerous therapeutic agent against Jab1 in gall bladder cancer.


Author(s):  
Pratibha Pandey ◽  
Uzma Sayyed ◽  
Rohit Tiwari ◽  
Neelam Pathak ◽  
Mohammad Haris Siddiqui ◽  
...  

Curcumin, the primary bioactive component isolated from turmeric, has been shown to possess variety of biologic functions including anti-cancer activity. However, meticulous mechanism of the curcumin in gall bladder cancer has not been explored yet. Therefore, in our study, we elucidated the mechanism of the anticancer action of curcumin against human gall bladder cancer cells. It was found that the curcumin treated GBC cells decreased cell viability in a dose and time-dependent manner. Nuclear condensation, Annexin V-FITC/PI positive cells, and caspase-3 activation confirmed the apoptotic induction due to anti-proliferative action of curcumin. Furthermore, curcumin induced disruption in the mitochondrial membrane potential and increased reactive oxygen species generation which has not yet been reported in earlier studies of curcumin with gall bladder cancer. Moreover, curcumin-induced apoptosis of gall bladder cancer cells was also accompanied by significant amount of growth arrest at the G0/G1 phase of the cell cycle which has also not been documented previously. To the best part of my knowledge, this study has established curcumin as one of the promising chemotherapeutic agent against gall bladder carcinoma. Thus the present study explored a novel mechanism explaining the anti cancerous effects of curcumin, and may provide an alternative therapeutic approach which can overcome the side effects of chemotherapy. Keywords: Gall bladder carcinoma Curcumin; Cell cycle analysis; Caspase-3; Apoptosis


2005 ◽  
Vol 173 (4S) ◽  
pp. 214-215 ◽  
Author(s):  
Daniel Cho ◽  
Xiao Fang Ha ◽  
J. Andre Melendez ◽  
Louis J. Giorgi ◽  
Badar M. Mian

2014 ◽  
Vol 05 (03) ◽  
pp. 246-252 ◽  
Author(s):  
Mumtaz Ahmad Ansari ◽  
Satyendra K. Tiwary ◽  
Uday Pratap Shahi ◽  
Vijay K. Shukla

2014 ◽  
Vol 13 (1) ◽  
pp. e514
Author(s):  
J. Mani ◽  
S. Vallo ◽  
S. Rakel ◽  
P. Antonietti ◽  
G. Bartsch ◽  
...  

Tumor Biology ◽  
2015 ◽  
Vol 36 (9) ◽  
pp. 7093-7098 ◽  
Author(s):  
Ehsan Hassan Hassan ◽  
Shawkat S. Gerges ◽  
Kamal A. El-Atrebi ◽  
Hala T. El-Bassyouni

2002 ◽  
Vol 167 (3) ◽  
pp. 1288-1294 ◽  
Author(s):  
OLIVIA ARANHA ◽  
LIPING ZHU ◽  
SAMIR ALHASAN ◽  
DAVID P. WOOD ◽  
TUAN H. KUO ◽  
...  

2011 ◽  
Vol 29 (7_suppl) ◽  
pp. 273-273
Author(s):  
H. Williams

273 Background: Muscle invasive bladder cancer portends a poor long term prognosis. Platinum based therapy is the mainstay of treatment but more effective agents are needed for management of this disease. Heat shock protein 90 (Hsp90) is a ubiquitous protein that has been shown to be overexpressed in tumor cells. It functions as a molecular chaperone responsible for the stability and function of a number of proteins critical to the oncogenic process. 17-(allylamino)-17 demethoxygeldanamycin (17 AAG) is a Hsp90 inhibitor that is currently in phase III trials in several tumor models. The purpose of this study was to evaluate the role of 17 AAG treatment for bladder cancer in vitro. Methods: Seven bladder cancer cell lines representing muscle invasive bladder cancer were treated in the presence and absence of 17 AAG. Both short term and long term treatments were evaluated for their effects on growth, motility and invasion of the cancer cells. Expression of proteins involved in cell growth, survival and metastasis were evaluated with Western blotting. Results: Our data demonstrated that 17 AAG treatment resulted in induction of apoptosis, inhibition of cell cycle progression through inhibition of MAP kinase pathway and cyclin D1 expression. Decreased tumor cell motility and invasion was observed with 17 AAG treatment. Several intracellular signaling pathways involved in cell proliferation, invasion and metastasis were inhibited. Conclusions: Hsp90 inhibition in muscle invasive bladder cancer cells impacts growth, motility and invasiveness by inhibiting numerous intracellular signaling pathways. Taken together, these findings suggest a possible role for Hsp90 inhibitors in bladder cancer tumorigenesis. No significant financial relationships to disclose.


2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e17028-e17028 ◽  
Author(s):  
Yuan-Ru Chen ◽  
Hsin-Chih Yeh ◽  
Fang-Yen Chiu ◽  
Hsin-En Wu ◽  
Huei-Chen Fang ◽  
...  

e17028 Background: Bladder cancer is one of the most common malignancies of urinary system with the forth incidence rate and the eighth leading mortality rate in male genitourinary tumors. Hypoxia environment activates the hypoxia‐signalling pathway, principally via hypoxia‐inducible transcription factors (HIF) to activate numerous target genes which mediate embryonic vascularization, metabolism, tumor angiogenesis and the other processes to supply tissues with blood and oxygen. Inflammasomes are multiprotein signal responsible for the maturation of proinflammatory cytokines IL-1β and IL-18 as well as trigger the inflammatory cell pyroptosis. Recent study showed that HIF-1α promotes NLRP3 inflammasome activation in bleomycin-induced acute lung injury. However, the role of HIF1α in regulating the progression of bladder cancer has not been examined so far. The present study aimed to investigate the effect of HIF-1α on NLRP3 inflammasome activation in urothelial carcinoma. Methods: In this research, urothelial carcinoma cell lines were treated with NLRP3 inflammasome inducers, LPS/ATP, to induce NLRP3 inflammasome activation. Results: Our preliminary results showed that both T24 and 5637 bladder cancer cells can be induced NLRP3 inflammasome activation and IL-1β secretion. In addition, hypoxia also induces the secretion of IL-1β in T24 cells. We further investigated the effect of NLRP3 inflammasome activation in modulating EMT-related protein levels, migration and invasion in bladder cancer T24 cells. Our results demonstrated that NLRP3 inflammasome activation promotes tumor growth and metastasis in bladder cancer cells. Furthermore, knockdown of HIF1α reduces both inflammatory response and migratory activity in bladder cancer. Conclusions: Collectively, these results suggest that targeting NLRP3 inflammasome might offer potential to treat hypoxic malignant tumor in bladder carcinoma.


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