Several transcription factors regulate COX-2 gene expression in pancreatic β-cells

Zhang, Xiongfei; Zhang, Jingjing; Yang, Xingsheng; Han, Xiao

doi:10.1007/s11033-007-9085-3

Cited by 31 publications

(33 citation statements)

References 63 publications

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“…In addition, IL-27-induced Th1 differentiation is dependent on activation of the MAPK pathway (37). Previous studies demonstrate that activation of STAT1 and inactivation of MAPK and PI3K/Akt pathways participate in the reduction of COX-2 expression (34,35,38,39). In this study, treatment of rIL-27 enhances the activation of STAT1 as well as the reduction of phosphorylation of ERK1/2 and NF-B (supplemental Fig.…”

Section: Discussionsupporting

confidence: 58%

IL-27 Directly Restrains Lung Tumorigenicity by Suppressing Cyclooxygenase-2-Mediated Activities

Leu

Sun

et al. 2009

The Journal of Immunology

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Gene transfer of IL-27 to tumor cells has been proven to inhibit tumor growth in vivo by antiproliferation, antiangiogenesis, and stimulation of immunoprotection. To investigate the nonimmune mechanism of IL-27 that suppresses lung cancer growth, we have established a single-chain IL-27-transduced murine Lewis lung carcinoma (LLC-1) cell line (LLC-1/scIL-27) to evaluate its tumorigenic potential in vivo. Mice inoculated with LLC/scIL-27 displayed retardation of tumor growth. Production of IL-12, IFN-γ, and cytotoxic T cell activity against LLC-1 was manifest in LLC/scIL-27-injected mice. Of note, LLC-1/scIL-27 exhibited decreased expression of cyclooxygenase-2 (COX-2) and PGE2. On the cellular level, the LLC/scIL-27 transfectants had reduced malignancy, including down-regulation of vimentin expression and reduction of cellular migration and invasion. The suppression of tumorigenesis by IL-27 on lung cancer cells was further confirmed by the treatment with rIL-27 on the murine LLC-1 and human non-small cell lung carcinoma (NSCLC) cell lines. PGE2-induced vimentin expression, movement, and invasiveness were also suppressed by the treatment with rIL-27. Our data show that IL-27 not only suppresses expression of COX-2 and PGE2 but also decreases the levels of vimentin and the abilities of cellular migration and invasion. Furthermore, inoculation of LLC/scIL-27 into immunodeficient NOD/SCID mice also exhibited reduced tumor growth. Our data indicate that IL-27-induced nonimmune responses can contribute to significant antitumor effects. Taken together, the results suggest that IL-27 may serve as an effective agent for lung cancer therapy in the future.

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Section: Discussionsupporting

confidence: 58%

IL-27 Directly Restrains Lung Tumorigenicity by Suppressing Cyclooxygenase-2-Mediated Activities

Leu

Sun

et al. 2009

The Journal of Immunology

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“…It is well established that chronic inflammation and associated COX-2 overexpression is an early event in the pathogenesis of “inflammation-related” cancers (63). COX-2 is transcriptionally regulated by STAT3, NF-κB and CREB; therefore, it is possible that Nexrutine® suppresses COX-2 by down regulation of these transcription factors in tumor cells (64, 65). Suppression of this signaling not only inhibits tumor cell growth it could potentially sensitize cancer cells to conventional treatment.…”

Section: Conclusion Future Directions and Challengesmentioning

confidence: 99%

Extracting the Benefit of Nexrutine® for Cancer Prevention

et al. 2015

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The current standard of care for prostate cancer includes hormone therapy, radiation therapy and radical prostatectomy, each with its own set of undesirable side effects. In this regard there is an unmet need to develop strategies that can prevent or delay the development of clinical prostate cancer. One potential area involves the use of natural compounds involving botanicals. Along these lines we have found that Nexrutine®, a dietary supplement derived from Phellodendron amurense bark extract, has prostate cancer prevention activity. The “extract” nature of this botanical, which constitutes a blend of several active protoberberine alkaloids, allows it to target several pathways deregulated in prostate cancer simultaneously. In this review, we will emphasize the prospective translational benefit of Nexrutine® as a chemopreventive agent for prostate cancer management. The potential of Nexrutine® was first identified and has subsequently been most exhaustively studied with reference to prostate cancer. Therefore the focus of this review is on the use of Nexrutine® in prostate cancer. In addition we have summarized the emerging evidence regarding the use of Nexrutine® in other tumor models to demonstrate the potential benefits of Nexrutine®.

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“…NF-kB and c-Jun participate in LPS-induced COX2 expression in mouse macrophages (Kang et al 2006). In rat insulinoma cells, CREB and the Ets family members Ets-1 and Elk-1 increase Cox2 promoter activity, while STAT1 inhibits Cox2 promoter activity (Zhang et al 2007). In human monocytes, ESE1 binds to and increases the activity of the COX2 promoter (Grall et al 2005).…”

Section: Figurementioning

confidence: 99%

COX2 and PGE2 mediate EGF-induced E-cadherin-independent human ovarian cancer cell invasion

Qiu¹,

Cheng²,

Chang³

et al. 2014

Endocrine-Related Cancer

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Elevated expression of cyclooxygenase 2 (COX2 (PTGS2)) has been reported to occur in human ovarian cancer and to be associated with poor prognosis. We have previously demonstrated that COX2-derived prostaglandin E2 (PGE2) promotes human ovarian cancer cell invasion. We had also demonstrated that epidermal growth factor (EGF) induces human ovarian cancer cell invasion by downregulating the expression of E-cadherin through various signaling pathways. However, it remains unclear whether COX2 and PGE2 are involved in the EGF-induced downregulation of E-cadherin expression and cell invasion in human ovarian cancer cells. In this study, we showed that EGF treatment induces COX2 expression and PGE2 production in SKOV3 and OVCAR5 human ovarian cancer cell lines. Interestingly, COX2 is not required for the EGF-induced downregulation of E-cadherin expression. In addition, EGF treatment activates the phosphatidylinositol-3-kinase (PI3K)/Akt and cAMP response element-binding protein (CREB) signaling pathways, while only the PI3K/Akt pathway is involved in EGF-induced COX2 expression. Moreover, we also showed that EGF-induced cell invasion is attenuated by treatment with a selective COX2 inhibitor, NS-398, as well as PGE2 siRNA. This study demonstrates an important role for COX2 and its derivative, PGE2, in the mediation of the effects of EGF on human ovarian cancer cell invasion.

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Several transcription factors regulate COX-2 gene expression in pancreatic β-cells

Cited by 31 publications

References 63 publications

IL-27 Directly Restrains Lung Tumorigenicity by Suppressing Cyclooxygenase-2-Mediated Activities

IL-27 Directly Restrains Lung Tumorigenicity by Suppressing Cyclooxygenase-2-Mediated Activities

Extracting the Benefit of Nexrutine® for Cancer Prevention

COX2 and PGE2 mediate EGF-induced E-cadherin-independent human ovarian cancer cell invasion

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