Essential role of c-Jun induction and coactivator p300 in epidermal growth factor-induced gene expression of cyclooxygenase-2 in human epidermoid carcinoma A431 cells

Chen, Lei Chin; Chen, Ben Kuen; Chang, Jia‐Wei; Chang, Wen Chang

doi:10.1016/j.bbalip.2004.04.003

Cited by 41 publications

(42 citation statements)

References 45 publications

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“…The stimulatory effect of I-BOP was significantly attenuated when both C/EBP and CRE sites were mutated (−207/+49 mCE/C) indicating that both C/EBP and CRE motifs are necessary for COX-2 promoter activation. These results demonstrated that C/EBP is more important in regulating the basal COX-2 expression, while CRE motif is more important in I-BOP response, analogous to that of EGF-induced COX-2 promoter activity in A431 cells [26].…”

Section: Cox-2 Promoter Luciferase Reporter Assaymentioning

confidence: 73%

“…The COX-2 promoter region does have one CRE, one C/EBP, and two NF-κB motifs which are responsible for the induced transcription of the COX-2 gene [26]. We investigated the role of CREB, C/EBP and NF-κB in the regulation of the transcription of COX-2 gene by I-BOP using luciferase reporter assay with different promoter deletion regions and mutation sites of COX-2 promoter.…”

Section: Discussionmentioning

confidence: 99%

“…Horseradish peroxidase (HRP)-linked goat anti-mouse and rabbit IgG were supplied by BD Transduction Laboratories (Lexington, KY). Luciferase reporter constructs with the different deletion regions from −918 to +49 bp and site-directed mutation of some consensus elements in COX-2 promoter were prepared as described previously [25,26].…”

Section: Methodsmentioning

confidence: 99%

“…After transfection for 16 h, cells were stimulated with 50 nM of I-BOP for additional 24 h. For inhibitor study, cells were pretreated with the respective inhibitors at working concentrations or vehicle (0.1% ethanol) for 30 min prior to I-BOP stimulation. The luciferase activity in cell lysate was determined as described previously [25,26].…”

Section: Transfection and Luciferase Reporter Gene Assaymentioning

confidence: 99%

“…In order to further investigate the transcriptional regulation of human COX-2 gene by I-BOP, the luciferase reporter bearing various lengths of 5′-flanking regions of COX-2 gene promoter were employed [26]. Because of low transfection efficiency of plasmids in A549 cells, COX-2 promoter assay was carried out in AD293-TPα cells which exhibited high transfection efficiency and were characterized previously ( AD293-TPα cells were transfected with various promoter constructs and the effect of I-BOP on the luciferase activity of these constructs was studied.…”

Section: Cox-2 Promoter Luciferase Reporter Assaymentioning

confidence: 99%

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Activation of thromboxane receptor α induces expression of cyclooxygenase-2 through multiple signaling pathways in A549 human lung adenocarcinoma cells

Wei

Yan

et al. 2007

Biochemical Pharmacology

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Human lung adenocarcinoma A549 cells stably transfected with TPα (A549-TPα) were used to study agonist I-BOP-induced expression of cyclooxygenase-2 (COX-2) and the related mechanisms of induced expression. I-BOP, a TP agonist, induced a time and dose dependent expression of COX-2 in A549-TPα cells as revealed by Western blot and by the synthesis of PGE 2 and TXB 2 which was totally inhibited by COX-2 inhibitors. The signaling pathways of I-BOP-induced COX-2 expression were elucidated by using various inhibitors of the signaling molecules. The effects of these inhibitors were assessed at three different levels of COX-2 expression: protein, enzyme activity and promoter activity. Within MAPK family, both ERK and p38 MAPK but not JNK/SAPK pathways were involved in the induction. Other pathways such as JAK/Stat3 pathway and β-catenin/TCF/LEF pathway also participated in the induction. The activation of key signaling molecules, ERK, p38 MAPK, CREB and NF-κB, involved in the COX-2 transcription was further studied at the phosphorylation step. Activation of ERK and p38 MAPK appeared to be mediated primarily by transactivation of EGFR, whereas activation of CREB and NF-κB was mediated by PKA, PKC and ERK. The role of CREB and NF-κB in I-BOP-induced COX-2 expression was further explored at the COX-2 promoter level. Studies on promoter fragments of different length and mutation of responsive motifs indicated that CRE and NF-κB sites are critical for the COX-2 induction. Distal NF-κB site is essential for the basal induction of the COX-2 transcription, whereas CRE and proximal NF-κB sites are important for the induced transcription. These results indicate that I-BOP induced COX-2 expression through multiple signaling pathways leading to the activation of CREB and NF-κB transcriptional factors and subsequent COX-2 transcription.

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Section: Cox-2 Promoter Luciferase Reporter Assaymentioning

confidence: 73%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Transfection and Luciferase Reporter Gene Assaymentioning

confidence: 99%

Section: Cox-2 Promoter Luciferase Reporter Assaymentioning

confidence: 99%

See 3 more Smart Citations

Activation of thromboxane receptor α induces expression of cyclooxygenase-2 through multiple signaling pathways in A549 human lung adenocarcinoma cells

Wei

Yan

et al. 2007

Biochemical Pharmacology

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Caveolin‐1 facilitates cyclooxygenase‐2 protein degradation

Chen

Liou

Huang

et al. 2009

J of Cellular Biochemistry

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Cyclooxygenase-2 (COX-2) plays major roles in diverse physiological and pathological processes such as inflammation and tumorigenesis. Transcriptional control of COX-2 has been extensively investigated and characterized, but its post-translational control is less clear. Here, we report a novel mechanism by which COX-2 is degraded. Protein levels of caveolin-1 (Cav-1) and COX-2 showed an inverse relation in colon cancer cell lines. COX-2 proteins in lung and colon tissues were higher in Cav-1 null mice than in wild-type mice. RNAi knockdown of Cav-1 increased COX-2 protein level and decreased ubiquitinated COX-2 accumulation. In addition, deletion of the carboxy (C)-terminus of COX-2, which contains a unique 19-amino acid segment compared with COX-1, resulted in reduced Cav-1 binding and attenuated COX-2 degradation. COX-1 and green fluorescence protein containing the C-terminus of COX-2 resulted in enhanced degradation. Our findings suggest that Cav-1 binds COX-2 in endoplasmic reticulum (ER) and carries it for degradation via ER associated degradation. The C-terminal region of COX-2 is required for Cav-1 binding and degradation. These results indicate a novel function of Cav-1 in controlling COX-2 expression, which may regulate physiological functions and have tumor suppression effects.

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Inhibition of LPS‐induced C/EBPδ by trichostatin a has a positive effect on LPS‐induced cyclooxygenase 2 expression in RAW264.7 cells

Liu

Wang

Hsu

et al. 2010

J of Cellular Biochemistry

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Cyclooxygenase 2 (COX-2) is an important inflammatory factor. Previous studies have indicated that COX-2 is induced with lipopolysaccharide (LPS) treatment. Here, we found that an inhibitor of histone deacetylase (HDAC), trichostatin A (TSA), cannot repress LPS-induced COX-2 but it increased the COX-2 level in RAW264.7 cells. We found no significant difference in NF-kappaB activation and ERK1/2 phosphorylation, but LPS-induced C/EBP delta expression was completely abolished after TSA treatment of LPS-treated cells. Interesting, reporter assay of C/EBP delta promoter revealed that Sp1-binding site is important. Although there was no alteration in c-Jun levels, but the phosphorylation of c-Jun at its C-terminus was increased dramatically. A DNA-associated protein assay (DAPA) and chromatin immunoprecipitation assay (ChIP) indicated that c-Jun was recruited via Sp1 to the promoter of C/EBP delta after LPS treatment; this recruitment of c-Jun was repressed by TSA. C/EBP delta inhibition by TSA resulted in increased binding of C/EBP alpha and C/EBP beta to the COX-2 promoter. Therefore, TSA has a positive effect on LPS-induced COX-2 since it decreases the C/EBP delta level by reducing c-Jun recruitment by Sp1 to the C/EBP delta promoter, resulting in increased the recruitment of C/EBP alpha and C/EBP beta to the COX-2 promoter.

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Essential role of c-Jun induction and coactivator p300 in epidermal growth factor-induced gene expression of cyclooxygenase-2 in human epidermoid carcinoma A431 cells

Cited by 41 publications

References 45 publications

Activation of thromboxane receptor α induces expression of cyclooxygenase-2 through multiple signaling pathways in A549 human lung adenocarcinoma cells

Activation of thromboxane receptor α induces expression of cyclooxygenase-2 through multiple signaling pathways in A549 human lung adenocarcinoma cells

Caveolin‐1 facilitates cyclooxygenase‐2 protein degradation

Inhibition of LPS‐induced C/EBPδ by trichostatin a has a positive effect on LPS‐induced cyclooxygenase 2 expression in RAW264.7 cells

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