scholarly journals COX-2 Inhibitors and Gastric Cancer

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Zhen Wang ◽  
Jun-qiang Chen ◽  
Jin-lu Liu
Keyword(s):  
Gastric Cancer ◽  
Antitumor Agents ◽  
Prostaglandin E ◽  
Potential Toxicity ◽  
Chemopreventive Agents ◽  
Treatment Regimens ◽  
Cox 2 ◽  
Cox 2 Inhibitors ◽  
Cancer Studies ◽  
Selection Of

The evidence that cyclooxygenase-2 (COX-2) is upregulated and plays an important role in carcinogenesis of gastric cancer has triggered the topic of COX-2 inhibitors as chemopreventive agents for gastric cancer. Studies find that COX-2 inhibitors are associated not only with chemoprophylactic effects, but also with chemotherapeutic potentials in gastric cancer. Both COX-dependent and COX-independent pathways have a role in the anticancer efficiency of COX-2 inhibitors. However, enthusiasm is thwarted by the potential toxicity, that is, gastrointestinal toxicity of nonselective COX-2 inhibitors and cardiovascular risk of selective COX-2 inhibitors. Therefore, more studies are needed to develop new targeted antitumor agents (such as prostaglandin E receptor antagonist) and to define fundamental questions such as optimal treatment regimens, integration of cotherapy, and careful selection of candidates.

Cyclooxygenase-2 inhibitors suppress the growth of gastric cancer xenografts via induction of apoptosis in nude mice

1998 ◽  
Vol 274 (6) ◽  
pp. G1061-G1067 ◽  
Author(s):  
Hitoshi Sawaoka ◽  
Sunao Kawano ◽  
Shingo Tsuji ◽  
Masahiko Tsujii ◽  
Edhi S. Gunawan ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Nude Mice ◽  
Tumor Volume ◽  
Malignant Tumors ◽  
Apoptotic Cell ◽  
Dependent Manner ◽  
Cox 2 ◽  
Induced Apoptosis ◽  
Cox 2 Inhibitors

To clarify the role of mitogen-inducible cyclooxygenase (COX-2) in the development of malignant tumors, we investigated the effects of COX-2 inhibitors on the growth of gastric cancer xenografts in nude mice in vivo. MKN45 gastric cancer cells (5 × 106cells/animal) that overexpress COX-2 were inoculated subcutaneously into athymic mice. NS-398, a specific COX-2 inhibitor, or indomethacin, a nonspecific COX-2 inhibitor, was administered orally to animals every day for 20 days. These drugs reduced the tumor volume significantly. Immunohistochemistry using bromodeoxyuridine, nick end labeling, and electron microscopy showed that NS-398 induced apoptosis in cancer cells in a dose-dependent manner and inhibited cancer cell replication slightly. Indomethacin also induced apoptosis and suppressed replication of tumor cells. There was a significant negative correlation between tumor volume and apoptotic cell number within the tumor. These results are consistent with the hypothesis that COX-2 inhibitors suppress growth of gastric cancer xenografts mainly by inducing apoptosis and suppressing replication of the neoplastic cells. It follows that COX-2 plays an important role in the development of gastric cancer.

scholarly journals Chlorinated cobalt alkyne complexes derived from acetylsalicylic acid as new specific antitumor agents

2018 ◽  
Vol 47 (12) ◽  
pp. 4341-4351 ◽  
Author(s):  
Victoria Obermoser ◽  
Daniel Baecker ◽  
Carina Schuster ◽  
Valentin Braun ◽  
Brigitte Kircher ◽  
...  
Keyword(s):  
Antitumor Agents ◽  
Tumor Cell Lines ◽  
Growth Inhibitory ◽  
Cox 2 ◽  
Alkyne Complexes ◽  
Inhibitory Potential ◽  
Cox 2 Inhibitors ◽  
Ht 29 ◽  
Cox 1 ◽  
Mcf 7

Chlorine-substituted [(prop-2-ynyl)-2-acetoxybenzoate]dicobalthexacarbonyl complexes are selective COX-2 inhibitors with growth-inhibitory potential against COX-1/2 containing MDA-MB-231 and HT-29 tumor cell lines. The metabolic activity of non-tumorigenic HS-5 cells and COX-1/2-independent MCF-7 cells is not influenced.

Chemoprevention of Gastric Cancer: Role of COX-2 Inhibitors and Other Agents

2004 ◽  
Vol 22 (4) ◽  
pp. 320-326 ◽  
Author(s):  
Gerardo Nardone ◽  
Alba Rocco
Keyword(s):  
Gastric Cancer ◽  
Cox 2 ◽  
Cox 2 Inhibitors

scholarly journals Inflammation in gastric cancer: Interplay of the COX‐2/prostaglandin E 2 and Toll‐like receptor/MyD88 pathways

2016 ◽  
Vol 107 (4) ◽  
pp. 391-397 ◽  
Author(s):  
Kanae Echizen ◽  
Osamu Hirose ◽  
Yusuke Maeda ◽  
Masanobu Oshima
Keyword(s):  
Gastric Cancer ◽  
Prostaglandin E ◽  
Toll Like Receptor ◽  
Cox 2

The Anti-Cancer Effect of COX-2 Inhibitors on Gastric Cancer Cells

2007 ◽  
Vol 52 (7) ◽  
pp. 1713-1721 ◽  
Author(s):  
Soo-Jeong Cho ◽  
Nayoung Kim ◽  
Joo Sung Kim ◽  
Hyun Chae Jung ◽  
In Sung Song
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Anti Cancer ◽  
Cox 2 ◽  
Cox 2 Inhibitors

scholarly journals Cyclooxygenase (COX)-2 modulates Toxoplasma gondii infection, immune response and lipid droplets formation in human trophoblast cells and villous explants

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Guilherme de Souza ◽  
Rafaela José Silva ◽  
Iliana Claudia Balga Milián ◽  
Alessandra Monteiro Rosini ◽  
Thádia Evelyn de Araújo ◽  
...  
Keyword(s):  
Immune Response ◽  
Toxoplasma Gondii ◽  
Inflammatory Cytokines ◽  
Lipid Droplets ◽  
Prostaglandin E ◽  
Trophoblast Cells ◽  
Human Trophoblast ◽  
Cox 2 ◽  
Cox 2 Inhibitors ◽  
Human Trophoblast Cells

AbstractCongenital toxoplasmosis is represented by the transplacental passage of Toxoplasma gondii from the mother to the fetus. Our studies demonstrated that T. gondii developed mechanisms to evade of the host immune response, such as cyclooxygenase (COX)-2 and prostaglandin E2 (PGE2) induction, and these mediators can be produced/stored in lipid droplets (LDs). The aim of this study was to evaluate the role of COX-2 and LDs during T. gondii infection in human trophoblast cells and villous explants. Our data demonstrated that COX-2 inhibitors decreased T. gondii replication in trophoblast cells and villous. In BeWo cells, the COX-2 inhibitors induced an increase of pro-inflammatory cytokines (IL-6 and MIF), and a decrease in anti-inflammatory cytokines (IL-4 and IL-10). In HTR-8/SVneo cells, the COX-2 inhibitors induced an increase of IL-6 and nitrite and decreased IL-4 and TGF-β1. In villous explants, the COX-2 inhibitors increased MIF and decreased TNF-α and IL-10. Furthermore, T. gondii induced an increase in LDs in BeWo and HTR-8/SVneo, but COX-2 inhibitors reduced LDs in both cells type. We highlighted that COX-2 is a key factor to T. gondii proliferation in human trophoblast cells, since its inhibition induced a pro-inflammatory response capable of controlling parasitism and leading to a decrease in the availability of LDs, which are essentials for parasite growth.

Inhibition of salivary secretion by lipopolysaccharide: possible role of prostaglandins

2001 ◽  
Vol 281 (2) ◽  
pp. E405-E411 ◽  
Author(s):  
A. Lomniczi ◽  
C. Mohn ◽  
A. Faletti ◽  
A. Franchi ◽  
S. M. McCann ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Salivary Secretion ◽  
Male Rats ◽  
Prostaglandin E ◽  
Synthesis Inhibitor ◽  
No Release ◽  
Cox 2 ◽  
Oxide Synthase ◽  
Cox 2 Inhibitors

Inducible (calcium-independent) nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) are important in the regulation of the function of different organs during infection. A single dose of lipopolysaccharide (LPS; 5 mg/kg ip) within 6 h increased NOS activity (20%) and prostaglandin E (PGE) content (100%) in submandibular glands (SMG) and blocked stimulated salivary secretion in adult male rats. The administration of an iNOS synthesis inhibitor, aminoguanidine (AG), with LPS decreased NOS activity and PGE content. Furthermore, the administration of meloxicam (MLX), an inhibitor of COX-2, blocked the increase in PGE and the production of NO. The incubation of slices of SMG in the presence of 3-morpholinosydnonimine, a donor of NO, increased the release of PGE highly significantly. The incubation of SMG in the presence of a PGE1 analog (alprostadil) increased the production of NO. These results indicate that LPS activates NOS, leading to NO release, which activates COX, generating PGEs that act back to further activate NOS, causing further generation of PGEs by activation of COX. Because the alprostadil administration inhibited stimulated salivation, LPS-induced inhibition of salivation appears to be caused by increased PGE production. Diminished salivary secretion produces poor oral health; thus the use of COX-2 inhibitors to counteract the effects of inhibited salivation should be considered.

scholarly journals Virtual Screening for Finding Novel COX-2 Inhibitors as Antitumor Agents

2012 ◽  
Vol 6 (1) ◽  
pp. 15-19 ◽  
Author(s):  
Zohreh S Badieyan ◽  
Seyed Adel Moallem ◽  
Soghra Mehri ◽  
Shabnam Shahsavand ◽  
Farzin Hadizadeh
Keyword(s):  
Virtual Screening ◽  
Antitumor Agents ◽  
Cox 2 ◽  
Cox 2 Inhibitors

scholarly journals Prognostic Significance of COX-2 Expression in Wilms' Tumor

2020 ◽  
Author(s):  
Onur Ceylan ◽  
Ozgur Caglar
Keyword(s):  
Wilms Tumor ◽  
Risk Group ◽  
Prognostic Significance ◽  
Risk Groups ◽  
Immunohistochemical Method ◽  
Prognostic Parameters ◽  
Treatment Regimens ◽  
Cox 2 ◽  
Almost All ◽  
Cox 2 Inhibitors

Objectives: In Wilms Tumor (WT) secondary malignancies caused by the side effects of intensive treatments remain one of the important problems. Therefore, there is a need for new studies to identify low- and high-risk groups for WT and to improve the treatment regimens of children in the low-risk group. Therefore, in our study, we aimed to determine the prognostic significance of the cyclooxygenase-2 (COX-2) biomarker in WT. Materials and Methods: Our study included 24 patients diagnosed with WT between January 2010 and December 2019. The correlation between COX-2 expression and significant prognostic parameters was investigated by studying COX-2 antibody using the immunohistochemical method. Results: COX-2 expression was observed in 22 of the patients, and the expression was more evident especially in the epithelial component. There was no significant correlation between COX-2 positivity and prognostic parameters. Conclusions: In our study, no significant relationship was found between significant prognostic parameters and COX-2 expression. We think that the COX-2 pathway is effective during the development phase of WT, since COX-2 expression was observed in almost all patients, therefore it may be beneficial to add COX-2 inhibitors to the treatment, and that a sufficient number of studies should be conducted in this respect.

Thrombin inhibits migration of human hepatic myofibroblasts

2007 ◽  
Vol 293 (1) ◽  
pp. G128-G136 ◽  
Author(s):  
Jennifer Gillibert-Duplantier ◽  
Véronique Neaud ◽  
Jean-Frédéric Blanc ◽  
Paulette Bioulac-Sage ◽  
Jean Rosenbaum
Keyword(s):  
Serine Proteinase ◽  
Receptor Activation ◽  
Fine Tuning ◽  
Prostaglandin E ◽  
Liver Myofibroblasts ◽  
Liver Fibrogenesis ◽  
Cox 2 ◽  
Β Receptor ◽  
Cox 2 Inhibitors

Several lines of data recently pointed out a role of the serine proteinase thrombin in liver fibrogenesis, but its mechanism of action is unknown. The aim of this study was to evaluate the effect of thrombin on the migration of human liver myofibroblasts. We show here that thrombin inhibits both basal migration and platelet-derived growth factor (PDGF)-BB-induced migration of myofibroblasts. By using a thrombin antagonist, a protease-activated receptor (PAR)-1 mimetic peptide, and a PAR-1 antibody, we show that this effect is dependent on the catalytic activity of thrombin and on PAR-1 activation. Thrombin's effect on basal migration was dependent on cyclooxygenase 2 (COX-2) activation because it was blocked by the COX-2 inhibitors NS-398 and nimesulide, and pharmacological studies showed that it was relayed through prostaglandin E2 and its EP2 receptor. On the other hand, thrombin-induced inhibition of PDGF-BB-induced migration was not dependent on COX-2. We show that thrombin inhibits PDGF-induced Akt-1 phosphorylation. This effect was consecutive to inhibition of PDGF-β receptor activation through active dephosphorylation. Thus thrombin, through two distinct mechanisms, inhibits both basal- and PDGF-BB-induced migration of human hepatic liver myofibroblasts. The fine tuning of myofibroblast migration may be one of the mechanisms used by thrombin to regulate liver fibrogenesis.

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