Signal transduction pathways regulating cyclooxygenase-2 expression: potential molecular targets for chemoprevention

Chun, Kyung‐Soo; Surh, Young‐Joon

doi:10.1016/j.bcp.2004.05.031

Cited by 373 publications

(297 citation statements)

References 136 publications

Supporting

Mentioning

282

Contrasting

Unclassified

Order By: Relevance

“…The two main reasons for this suggestion are: (i) COX-2 is overexpressed in a variety of tumors, which have profoundly increased synthesis of prostaglandins; (ii) COX-2 exhibits a strong anti-apoptotic activity via prostaglandin synthesis [29,71,85]. There are certain limitations for the direct application of this approach to the treatment of melanomas; COX-2 is present in most melanomas at a moderate level, and COX-2 inhibitors alone do not induce apoptosis in this type of tumors.…”

Section: Discussionmentioning

confidence: 99%

Dual treatment with COX-2 inhibitor and sodium arsenite leads to induction of surface Fas Ligand expression and Fas-Ligand-mediated apoptosis in human melanoma cells

Ivanov¹,

Hei²

2006

Experimental Cell Research

View full text Add to dashboard Cite

Most human melanomas express Fas receptor on the cell surface, and treatment with exogenous Fas Ligand (FasL) efficiently induces apoptosis of these cells. In contrast, endogenous surface expression of FasL is suppressed in Fas-positive melanomas. We report here the use of a combination of sodium arsenite, an inhibitor of NF-κB activation, and NS398, a cyclooxygenase-2 (COX-2) inhibitor, for restoration of the surface FasL expression. We observed a large increase of Fas-mediated apoptosis in Fas-positive melanomas. This was due to induction of FasL surface expression and increased susceptibility to Fas death signaling after arsenite and NS398 treatment. Furthermore, silencing COX-2 expression by specific RNAi also effectively increased surface FasL expression following arsenite treatment. Upregulation of the surface FasL levels was based on an increase in the efficiency of translocation to the cell surface and stabilization of FasL protein on the cell surface, rather than on acceleration of the FasL gene transcription. Data obtained demonstrate that the combination of arsenite with inhibitors of COX-2 may affect the target cancer cells via induction of FasL-mediated death signaling.

show abstract

Section: Discussionmentioning

confidence: 99%

Dual treatment with COX-2 inhibitor and sodium arsenite leads to induction of surface Fas Ligand expression and Fas-Ligand-mediated apoptosis in human melanoma cells

Ivanov¹,

Hei²

2006

Experimental Cell Research

View full text Add to dashboard Cite

show abstract

“…In this study, we demonstrated for the first time that Foxm1 plays a role in chronic lung inflammation, a known predisposing factor for tumor development. Although pulmonary inflammation was completely resolved by 12 weeks after initiation of MCA/BHT treatment in WT mice, Rosa26-Foxm1 mice displayed persistent pulmonary inflammation, macrophage infiltration, and increased expression of genes essential for pulmonary inflammation and remodeling in response to lung injury (Bratt, 2000;Wolters and Chapman, 2000;Chun and Surh, 2004;Kulbe et al, 2004;Riedl et al, 2004;Acuff et al, 2006). Therefore, the observed changes in gene expression probably represent the increased inflammatory response in MCA/BHT-treated Rosa26-Foxm1 lungs compared to WT lungs.…”

Section: Foxm1 Induces Formation Of Lung Tumors I-c Wang Et Almentioning

confidence: 99%

“…Interestingly, by 24 weeks after tumor initiation, expression levels of these genes were decreased in the Rosa26-Foxm1 lungs to approximately WT levels ( Figure 3). Furthermore, lungs from MCA/BHT-treated Rosa26-Foxm1 mice displayed a significant increase in expression levels of Rosa26-Foxm1 transgenic lungs exhibit elevated Cox-2 levels Previous studies demonstrated that the expression of Cyclooxygenese-2 (Cox-2) is induced during pulmonary inflammation and lung carcinogenesis (Chun and Surh, 2004;Riedl et al, 2004). Since microarray analysis revealed increased Cox-2 levels in MCA/BHT-treated Rosa26-Foxm1 lungs (Table 2), we hypothesized that Foxm1 directly or indirectly regulates Cox-2 expression.…”

Section: Foxm1 Induces Formation Of Lung Tumors I-c Wang Et Almentioning

confidence: 99%

“…Sustained inflammation and increased tumorigenesis in Rosa26-Foxm1 lungs was associated with increased expression of Cox-2, a well-known marker of inflammation and a critical player in carcinogenesis Foxm1 induces formation of lung tumors I-C Wang et al (Chun and Surh, 2004;Riedl et al, 2004). Elevated Cox-2 expression has been found in a variety of human cancers including NSCLC (Chun and Surh, 2004;Riedl et al, 2004).…”

Section: Foxm1 Induces Formation Of Lung Tumors I-c Wang Et Almentioning

confidence: 99%

See 1 more Smart Citation

Transgenic expression of the forkhead box M1 transcription factor induces formation of lung tumors

et al. 2008

View full text Add to dashboard Cite

The forkhead box m1 (Foxm1 or Foxm1b) protein (previously called HFH-11B, Trident, Win or MPP2) is abundantly expressed in human non-small cell lung cancers where it transcriptionally induces expression of genes essential for proliferation of tumor cells. In this study, we used Rosa26-Foxm1 transgenic mice, in which the Rosa26 promoter drives ubiquitous expression of Foxm1 transgene, to identify new signaling pathways regulated by Foxm1. Lung tumors were induced in Rosa26-Foxm1 mice using the 3-methylcholanthrene (MCA)/butylated hydroxytoluene (BHT) lung tumor initiation/promotion protocol. Tumors from MCA/BHTtreated Rosa26-Foxm1 mice displayed a significant increase in the number, size and DNA replication compared to wild-type mice. Elevated tumor formation in Rosa26-Foxm1 transgenic lungs was associated with persistent pulmonary inflammation, macrophage infiltration and increased expression of cyclooxygenase-2 (Cox-2), Cdc25C phosphatase, cyclin E2, chemokine ligands CXCL5, CXCL1 and CCL3, cathepsins and matrix metalloprotease-12. Cell culture experiments with A549 human lung adenocarcinoma cells demonstrated that depletion of Foxm1 by either short interfering RNA transfection or treatment with Foxm1-inhibiting ARF 26-44 peptide significantly reduced Cox-2 expression. In co-transfection experiments, Foxm1 protein-induced Cox-2 promoter activity and directly bound to the À2566/ À2580 bp region of human Cox-2 promoter.

show abstract

“…An interesting strategy for targeting the cancer cells includes the use of chemicals, dietary biofactors, phytochemicals and even whole plant extracts to thwart the progress of cancers by halting/reversing tumor promotion/progression [4][5][6]. Previously, the anti-carcinogenetic properties of phytochemicals such as resveratrol, gingerol, caffeic acid phenyl ester or genistein were established in many different studies.…”

Section: Introductionmentioning

confidence: 99%

Apoptotic effects of non-edible parts of Punica granatum on human multiple myeloma cells

et al. 2015

View full text Add to dashboard Cite

Multiple myeloma is of great concern since existing therapies are unable to cure this clinical condition. Alternative therapeutic approaches are mandatory, and the use of plant extracts is considered interesting. Punica granatum and its derived products were suggested as potential anticancer agents due to the presence of bioactive compounds. Thus, polypenolic-rich extracts of the non-edible parts of P. granatum were investigated for their antiproliferative and apoptotic effects on U266 multiple myeloma cells. We demonstrated that there were dose-dependent decreases in the proliferation of U266 cells in response to P. granatum extracts. Also, exposure to the extracts triggered apoptosis with significant increases in loss of mitochondrial membrane potential in U266 cells exposed to the leaves and stem extracts, while the flower extract resulted in slight increases in loss of MMP. These results were confirmed by Annexin-V analysis. These results documented the cytotoxic and apoptotic effects of P. granatum extracts on human U266 multiple myeloma cells via disruption of mitochondrial membrane potential and increasing cell cycle arrest. The data suggest that the extracts can be envisaged in cancer chemoprevention and call for further exploration into the potential application of these plant parts.

show abstract

Signal transduction pathways regulating cyclooxygenase-2 expression: potential molecular targets for chemoprevention

Cited by 373 publications

References 136 publications

Dual treatment with COX-2 inhibitor and sodium arsenite leads to induction of surface Fas Ligand expression and Fas-Ligand-mediated apoptosis in human melanoma cells

Dual treatment with COX-2 inhibitor and sodium arsenite leads to induction of surface Fas Ligand expression and Fas-Ligand-mediated apoptosis in human melanoma cells

Transgenic expression of the forkhead box M1 transcription factor induces formation of lung tumors

Apoptotic effects of non-edible parts of Punica granatum on human multiple myeloma cells

Contact Info

Product

Resources

About