Targeting of COX-2 Expression by Recombinant Adenovirus shRNA Attenuates the Malignant Biological Behavior of Breast Cancer Cells

Tu, Bo; Ma, Tingting; Peng, Xueqing; Wang, Qin; Yang, Hong; Huang, Xiaoling

doi:10.7314/apjcp.2014.15.20.8829

Cited by 8 publications

(5 citation statements)

References 43 publications

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“…Pro-inflammatory cytokines, growth factors, bile acids, ultraviolet B irradiation are stimulators of COX-2 expression. Cyclooxygenase-2 contributes to disease processes, including cancer and inflammation (Kim et al, 2011;Tu et al, 2014). Cyclooxygenase can convert pro-carcinogens to carcinogens and can co-oxidase xenobiotics into mutagens by its peroxidase activity.…”

Section: Discussionmentioning

confidence: 99%

Effects of a Multikinase Inhibitor Motesanib (AMG 706) Alone and Combined with the Selective DuP-697 COX-2 Inhibitor on Colorectal Cancer Cells

Kaya¹,

Altun²,

Turgut³

et al. 2016

Asian Pacific Journal of Cancer Prevention

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In the present study, we investigated the effects of motesanib (AMG 706), a multikinase inhibitor alone and in combination with DuP-697, an irreversible selective inhibitor of COX-2, on cell proliferation, angiogenesis, and apoptosis induction in a human colorectal cancer cell line (HT29). Real time cell analysis (RTCA, Xcelligence system) was used to determine the effects on colorectal cancer cell proliferation. Apoptosis was assessed with annexin V staining and angiogenesis was determined with chorioallantoic membrane model. We found that motesanib alone exerted antiproliferative, antiangiogenic and apoptotic effects on HT29 colorectal cancer cells. Combination with DUP-697 increased the antiproliferative, antiangiogenic and apoptotic effects. Results of this study indicate that motesanib may be a good choice in treatment of colorectal tumors. In addition, the increased effects of combination of motesanib with DuP-697 raise the possibility of using lower doses of these drugs and therefore avoid/minimize the dose-dependent side effects generally observed.

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Section: Discussionmentioning

confidence: 99%

Effects of a Multikinase Inhibitor Motesanib (AMG 706) Alone and Combined with the Selective DuP-697 COX-2 Inhibitor on Colorectal Cancer Cells

Kaya¹,

Altun²,

Turgut³

et al. 2016

Asian Pacific Journal of Cancer Prevention

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“…COX-2 mediates synthesis of prostaglandins (including PGE 2 ) and thromboxanes that promote cytokine secretion and suppresses immune function by inhibition of T H 1 cell activation and IL-2 secretion. Up-regulation of COX-2 has been reported to play a key role in regulating inflammatory responses that causes tissue injury in numerous cancers (Tu et al, 2014). Thus, the identification of a novel COX-2 inhibitor could be useful in helping to protect patients against chronic inflammatory disorders.…”

Section: Discussionmentioning

confidence: 99%

Acacia ferrugineainhibits inflammation by regulating inflammatory iNOS and COX-2

Sakthivel

Guruvayoorappan

2015

Journal of Immunotoxicology

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Inflammation is a local defensive reaction of a host to cellular injury or infection. Prolonged inflammation can contribute to pathogenesis of many disorders. Identification of naturally occurring phytoconstituents that can suppress inflammatory mediators can lead to the discovery of anti-inflammatory therapeutics. Acacia ferruginea is used traditionally to treat numerous ailments including hemorrhage, irritable bowel syndrome and leprosy. The present study evaluated the anti-inflammatory activity of A. ferruginea extract against acute (carrageenan) and chronic (formaldehyde) inflammation in Balb/c mice. Pre-treatment with A. ferruginea extract (10 mg/kg BW) for 5 consecutive days via intraperitonial (IP) administration significantly inhibited subsequent induction of paw edema in both models; the effects were comparable to that of the standard drug indomethacin. The results also showed the A. ferruginea extract significantly inhibited nitric oxide (NO) synthesis and iNOS expression (as measured in serum), diminished inflammation in -and neutrophil infiltration to -the paw tissues and led to a reduction in the number of COX-2 + immunoreative cells (as evidenced by histologic and immunohistochemical analyses) in the paws relative to those in paws of mice that received the irritants only. Further, in vitro studies showed the extract could significantly scavenge free radicals generated as in DPPH and NO radical generating assays. Taken together, the results showed that A. ferruginea extract imparted potent anti-oxidant and -inflammatory effects, in part by maintaining oxidative homeostasis, inhibiting NO synthesis and suppressing iNOS and COX-2 expression and so could potentially be exploited as a potential plant-based medication against inflammatory disorders.

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“…Numerous studies have shown a link between COX-2/PGE 2 and Wnt/β-catenin signaling in development of many cancers, including lung cancer (Singh and Katiyar, 2013), skin cancer (Prasad and Katiyar, 2014), breast cancer (Tu et al, 2014), colorectal cancer (Castellone et al, 2005), and neuroblastoma (Jansen et al, 2015). In addition, a number of studies have shown that the COX-2/PGE 2 /β-catenin signaling pathway may be a potential target to inhibit cancer cell growth and migration.…”

Section: Discussionmentioning

confidence: 99%

Moringa oleifera Alkaloids Inhibited PC3 Cells Growth and Migration Through the COX-2 Mediated Wnt/β-Catenin Signaling Pathway

Xie¹,

Luo²,

Shi³

et al. 2020

Front. Pharmacol.

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Moringa oleifera Lam. (M. oleifera) is valuable plant distributed in many tropical and subtropical countries. It has a number of medicinal uses and is highly nutritious. M. oleifera has been shown to inhibit tumor cell growth, but this effect has not been demonstrated on prostate cancer cells. In this study, we evaluated the inhibitory effect of M. oleifera alkaloids (MOA) on proliferation and migration of PC3 human prostate cancer cells in vitro and in vivo. Furthermore, we elucidated the mechanism of these effects. The results showed that MOA inhibited proliferation of PC3 cells and induced apoptosis and cell cycle arrest. Furthermore, MOA suppressed PC3 cell migration and inhibited the expression of matrix metalloproteinases (MMP)-9. In addition, MOA significantly downregulated the expression of cyclooxygenase 2 (COX-2), β-catenin, phosphorylated glycogen synthase 3β, and vascular endothelial growth factor, and suppressed production of prostaglandin E2 (PGE2). Furthermore, FH535 (β-catenin inhibitor) and MOA reversed PGE2-induced PC3 cell proliferation and migration, and the effects of MOA and FH535 were not additive. In vivo experiments showed that MOA (150 mg/kg) significantly inhibited growth of xenograft tumors in mice, and significantly reduced the protein expression levels of COX-2 and β-catenin in tumor tissues. These results indicate that MOA inhibits the proliferation and migration, and induces apoptosis and cell cycle arrest of PC3 cells. Additionally, MOA inhibits the proliferation and migration of PC3 cells through suppression of the COX-2 mediated Wnt/β-catenin signaling pathway.

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Targeting of COX-2 Expression by Recombinant Adenovirus shRNA Attenuates the Malignant Biological Behavior of Breast Cancer Cells

Cited by 8 publications

References 43 publications

Effects of a Multikinase Inhibitor Motesanib (AMG 706) Alone and Combined with the Selective DuP-697 COX-2 Inhibitor on Colorectal Cancer Cells

Effects of a Multikinase Inhibitor Motesanib (AMG 706) Alone and Combined with the Selective DuP-697 COX-2 Inhibitor on Colorectal Cancer Cells

Acacia ferrugineainhibits inflammation by regulating inflammatory iNOS and COX-2

Moringa oleifera Alkaloids Inhibited PC3 Cells Growth and Migration Through the COX-2 Mediated Wnt/β-Catenin Signaling Pathway

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