Decisive role of cyclooxygenase-2 and lipocalin-type prostaglandin D synthase in chemotherapeutics-induced apoptosis of human cervical carcinoma cells

@article{Eichele2008DecisiveRO,
  title={Decisive role of cyclooxygenase-2 and lipocalin-type prostaglandin D synthase in chemotherapeutics-induced apoptosis of human cervical carcinoma cells},
  author={K. Eichele and R. Ramer and B. Hinz},
  journal={Oncogene},
  year={2008},
  volume={27},
  pages={3032-3044}
}
The role of cyclooxygenase-2 (COX-2) in cancer remains controversial. Using cervical carcinoma cells (HeLa), the present study investigates the involvement of COX-2 in apoptosis elicited by the chemotherapeutics paclitaxel, cisplatin and 5-fluorouracil. Each compound led to a profound induction of COX-2 expression and prostaglandin (PG) synthesis, accompanied by a substantial decrease of viability and enhanced apoptosis. Cells were significantly less sensitive to apoptotic death when either COX… Expand
R(+)-Methanandamide-Induced Apoptosis of Human Cervical Carcinoma Cells Involves A Cyclooxygenase-2-Dependent Pathway
TLDR
This study demonstrates COX-2 induction and synthesis of L-PGDS-derived, PPARγ-activating PGs as a possible mechanism of apoptosis by MA. Expand
Lovastatin lactone elicits human lung cancer cell apoptosis via a COX-2/PPARγ-dependent pathway
TLDR
COx-2 induction and subsequent COX-2-dependent activation of PPARγ is demonstrated as a hitherto unknown mechanism by which lovastatin lactone induces human lung cancer cell death. Expand
Induction but not inhibition of COX-2 confers human lung cancer cell apoptosis by celecoxib
TLDR
A COX-2- and PPARγ-dependent cytotoxic action of celecoxib was proven for primary human lung tumor cells and a proapoptotic mechanism of cele Coxib involving initial upregulation of COx-2 and PParγ and a subsequent nuclear translocation of PPAR γ by COX -2-dependent PGs is demonstrated. Expand
COX-2 and PPAR-γ Confer Cannabidiol-Induced Apoptosis of Human Lung Cancer Cells
TLDR
In lung cancer cell lines and primary cells from a patient with lung cancer, cannabidiol elicited decreased viability associated with apoptosis and caused upregulation of COX-2 and PPAR-γ in tumor tissue and tumor regression that was reversible by GW9662. Expand
Cancer Therapeutic Insights COX-2 and PPAR-g Confer Cannabidiol-Induced Apoptosis of Human Lung Cancer Cells
The antitumorigenicmechanismof cannabidiol is still controversial. This study investigates the role of COX2 and PPAR-g in cannabidiol’s proapoptotic and tumor-regressive action. In lung cancer cellExpand
Enhanced 5-fluorouracil cytotoxicity in high cyclooxygenase-2 expressing colorectal cancer cells and xenografts induced by non-steroidal anti-inflammatory drugs via downregulation of dihydropyrimidine dehydrogenase
TLDR
Collagen IV up-regulated significantly the COX-2 and DPD mRNA, and protein expressions, and also their enzyme activities in HT-29 cells, which enhanced in a synergistic manner the cytotoxic effect of 5-FU treatment both in vitro and in vivo. Expand
Mechanism of P-glycoprotein expression in the SGC7901 human gastric adenocarcinoma cell line induced by cyclooxygenase-2.
  • K. Gu, Y. Chen
  • Biology, Medicine
  • Asian Pacific journal of cancer prevention : APJCP
  • 2012
TLDR
COX-2 may induce the expression of P-gp in SGC7901 cell line via the NF-kappa B pathway with pacliaxel stimulation with dose- dependence. Expand
Diminished lipocalin-type prostaglandin D(2) synthase expression in human lung tumors.
TLDR
It is concluded that L-PGDS may play a key role in modulating lung cancer growth and may offer a novel diagnostic and therapeutic approach for treatment. Expand
Modulation of mammary cancer cell migration by 15-deoxy-delta(12,14)-prostaglandin J(2): implications for anti-metastatic therapy.
TLDR
The results of the present study suggest that electrophiles such as 15d-PGJ2 are potential anti-metastatic agents which exhibit specificity for migration and adhesion pathways at low concentrations where there are no observed effects on Keap1 or cytotoxicity. Expand
Celecoxib antagonizes perifosine's anticancer activity involving a cyclooxygenase-2-dependent mechanism
TLDR
A novel mechanism underlying the anticancer activity of perifosine that involves the induction of cyclooxygenase 2 (COX-2) in human cancer cells is revealed, indicating that the activation of COx-2 contributes to the antic cancer activity ofperifosines. Expand
...
1
2
3
...

References

SHOWING 1-10 OF 31 REFERENCES
Prostaglandin D2 and J2 induce apoptosis in human leukemia cells via activation of the caspase 3 cascade and production of reactive oxygen species
TLDR
The presence of prostaglandins (PGs) has been demonstrated in the processes of carcinogenesis and inflammation and a differential apoptotic effect of PGs through ROS production, followed by activation of the caspase 3 cascade, was demonstrated. Expand
Up-Regulation of Cyclooxygenase-2 Expression Is Involved in R(+)-Methanandamide-Induced Apoptotic Death of Human Neuroglioma Cells
TLDR
COX-2 is defined as a hitherto unknown target by which a cannabinoid induces apoptotic death of glioma cells and the data show that pharmacological concentrations of celecoxib may interfere with the proapoptotic action of R(+)-MA and anandamide, suggesting that cotreatment with COx-2 inhibitors could diminishglioma regression induced by these compounds. Expand
Suppression of chondrosarcoma cells by 15-deoxy-Delta 12,14-prostaglandin J2 is associated with altered expression of Bax/Bcl-xL and p21.
TLDR
The results of the current study suggest that the potential ability of 15d-PGJ(2) in regulation of cell cycle and inhibition of Bcl-xL expression might be beneficial in the development of novel pharmacological agents for chondrosarcoma. Expand
Induction of G0/G1 cell cycle arrest in ovarian carcinoma cells by the anti-inflammatory drug NS-398, but not by COX-2-specific RNA interference
TLDR
The experiments suggest that NS-398 reduced cell proliferation in ovarian carcinoma cells by induction of G0/G1 cell cycle arrest independent of COX-2 inhibition, and shows that specific inhibition ofCOX isoforms by RNAi could be used to dissociate effects of NSAIDs. Expand
Increase in PGE2 biosynthesis induces a Bax dependent apoptosis correlated to patients’ survival in glioblastoma multiforme
TLDR
It is shown that PGE2 physically associates with Bax, triggering its apoptotic-like change in conformation and its subsequent association with mitochondria, which induced a dose-dependent apoptosis in GBM cultures, which was dependent on the presence of Bax. Expand
R(+)-Methanandamide Elicits a Cyclooxygenase-2-Dependent Mitochondrial Apoptosis Signaling Pathway in Human Neuroglioma Cells
TLDR
R(+)-MA-induced apoptosis is mediated via a mitochondrial-dependent pathway that becomes activated, at least in part, through up-regulation of the COX-2 enzyme. Expand
Overexpression of COX-2 in human osteosarcoma cells decreases proliferation and increases apoptosis.
TLDR
The results suggest that COX-2 overexpression in osteosarcoma cells may increase resistance to tumorigenesis by increasing ROS to levels that decrease cell viability and the effects of COX -2 overeexpression are cell type/tissue dependent. Expand
Targeting Cyclooxygenase-2 in Recurrent Non–Small Cell Lung Cancer: A Phase II Trial of Celecoxib and Docetaxel
TLDR
It is suggested that combining celecoxib with docetaxel using the doses and schedule employed does not improve survival in unselected patients with recurrent, previously treated NSCLC, and further investigation of strategies designed to decrease PGE2 synthesis inNSCLC seems warranted. Expand
Ceramide is involved in r(+)-methanandamide-induced cyclooxygenase-2 expression in human neuroglioma cells.
TLDR
Results demonstrate that R(+)-MA induces COX-2 expression in human neuroglioma cells via synthesis of ceramide and subsequent activation of p38 and p42/44 MAPK pathways. Expand
Tumorigenic Transformation of Immortalized ECV Endothelial Cells by Cyclooxygenase-1 Overexpression*
TLDR
Cox-1 overexpression in immortalized ECV endothelial cells results in nuclear localization of the polypeptide and tumorigenesis, suggesting a nonprostanoid function of Cox-1. Expand
...
1
2
3
4
...