Induction of COX-2 protein expression by vanadate in A549 human lung carcinoma cell line through EGF receptor and p38 MAPK-mediated pathway

Chien, Pei Shan; Mak, Oi Tong; Huang, Hao

doi:10.1016/j.bbrc.2005.11.045

Cited by 57 publications

(34 citation statements)

References 49 publications

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“…Nowadays there are many unresolved questions concerning the relationship between apoptosis and the generation of ROS, such as which ROS are involved in apoptosis, what mechanisms and targets are important and whether apoptosis is triggered by ROS damage or if they are generated as a consequence of the cellular disruption that occurs during cell death [65]. It has been shown that vanadium-induced oxidative stress leads different cellular types to death by apoptotic and/or necrotic processes [11,66,67] as it was observed for V(V)-Salsem.…”

Section: Discussionmentioning

confidence: 99%

Biological effects of a complex of vanadium(V) with salicylaldehyde semicarbazone in osteoblasts in culture: Mechanism of action

Rivadeneira

Barrio

Arrambide

et al. 2009

Journal of Inorganic Biochemistry

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Section: Discussionmentioning

confidence: 99%

Biological effects of a complex of vanadium(V) with salicylaldehyde semicarbazone in osteoblasts in culture: Mechanism of action

Rivadeneira

Barrio

Arrambide

et al. 2009

Journal of Inorganic Biochemistry

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“…p38 MAPK plays an important role in the expression of proinflammatory molecules and the regulation of cellular responses during infection and has been widely investigated for an effect on COX-2 at translational and transcriptional levels. 28 Interleukin (IL)-1␤-induced transcription of COX-2 in a human microvascular endothelial cell line has been shown to require the combinatorial action of transcription factors, such as activated protein-2 (AP2), nuclear factor-IL-6 (NF-IL-6), and cAMP-responsive elements (CRE). 29 The CRE element in the COX-2 promoter is necessary for the induction of COX-2 transcription mediated by nitric oxide, proteasome inhibitors, and lipopolysaccharide (LPS).…”

Section: Discussionmentioning

confidence: 99%

Acrolein Induces Cyclooxygenase-2 and Prostaglandin Production in Human Umbilical Vein Endothelial Cells

Park

Kim

Misonou

et al. 2007

ATVB

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Objective-Acrolein, a known toxin in tobacco smoke, might be involved in atherogenesis. This study examined the effect of acrolein on expression of cyclooxygenase-2(COX-2) and prostaglandin (PG) production in endothelial cells. Methods and Results-Cyclooxygenase (COX)-2 induction by acrolein and signal pathways were measured using Western blots, Northern blots, immunoflouresence, ELISA, gene silencing, and promoter assay. Colocalization of COX2 and acrolein-adduct was determined by immunohistochemistry. Here we report that the levels of COX-2 mRNA and protein are increased in human umbilical vein endothelial cells (HUVECs) after acrolein exposure. COX-2 was found to colocalize with acrolein-lysine adducts in human atherosclerotic lesions. Inhibition of p38 MAPK activity abolished the induction of COX-2 protein and PGE 2 accumulation by acrolein, while suppression of extracellular signal-regulated kinase (ERK) and JNK activity had no effect on the induction of COX-2 expression in experiments using inhibitors and siRNA. Furthermore, rottlerin, an inhibitor of protein kinase C␦ (PKC␦), abrogated the upregulation of COX-2 at both protein and mRNA levels. Conclusion-These results provide that acrolein may play a role in progression of atherosclerosis and new information on the signaling pathways involved in COX-2 upregulation in response to acrolein and provide evidence that PKC␦ and p38 MAPK are required for transcriptional activation of COX-2. Key Words: acrolein Ⅲ COX-2 Ⅲ p38 MAPK Ⅲ atherosclerosis Ⅲ endothelial cells A ctivation of endothelial cells by proinflammatory stimuli has been established as an important link between risk factors and the pathologic mechanisms underlying atherosclerosis. 1 Thus, control of the inflammatory status of endothelial cells, which is achieved by a balance of pro-and antiinflammatory signals, is crucial to limiting the disease. Tobacco smoking induces inflammatory reactions 2 and promotes atherosclerosis 3 ; however, the mechanism that links cigarette smoking to an increased incidence of atherosclerosis is poorly understood.Acrolein (CH 2 ϭCH-CHO), a major product of organic combustion, including tobacco smoking, is the most reactive ␣, ␤-unsaturated aldehyde found widely in the environmol/ Lent. Acrolein is highly reactive and is hazardous to human health. 4 Acrolein is produced by a wide variety of both natural and synthetic processes, including the incomplete combustion of organic materials. Acrolein also has been found to be formed from threonine by neutrophil myeloperoxidase at sites of inflammation 5 and has been identified as both a product and initiator of lipid peroxidation. 6 Recent studies have shown that acrolein levels are increased in many diseases such as atherosclerosis, Alzheimer disease, and diabetes, and is possibly related to pathogenesis in these conditions. 7-9 We and others have reported that acrolein elevates intracellular reactive oxygen species (ROS) levels, which leads to cell dysfunction. 8,10 ROS-mediated cell damage is an important etiologic factor ...

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“…[3][4][5][6] The uniqueness of vanadium is that it is a micronutrient and is included in the list of 40 essential micronutrients that are required in small amounts for normal metabolism. Accordingly, it has been incorporated in many multinational pharmaceutical preparations along with vitamins and other trace elements for maintenance of normal health.…”

mentioning

confidence: 99%

Suppression of cell proliferation, induction of apoptosis and cell cycle arrest: Chemopreventive activity of vanadium in vivo and in vitro

Ray

Ghosh

Rana

et al. 2006

Intl Journal of Cancer

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In the present study, the authors evaluated the anticancer mechanism of vanadium, a dietary micronutrient and an important pharmacological agent, on a defined model of chemically induced rat mammary carcinogenesis in vivo and on human breast cancer cell line MCF7 in vitro. Female Sprague-Dawley rats were treated with 7,12-dimethylbenz(a)anthracene (0.5 mg/100 g body weight) by a single tail vein injection in an oil emulsion to induce mammary preneoplasia. Vanadium (ammonium monovanadate) at a concentration of 0.5 ppm (4.27 lmol/l) was supplemented in drinking water and given ad libitum to the experimental groups for 24 weeks. Histological finding showed substantial repair of hyperplastic lesions. There was a significant reduction in incidence, multiplicity (34%, p < 0.01), size of palpable mammary tumors and delay in mean latency period of tumor appearance. Immunohistochemical analysis in vivo indicated a decrease in cell proliferation (24.68% p < 0.05) and an increase among the TUNEL-positive apoptotic cells along with strong expressions of p53 and Bax, and downregulation of Bcl2 proteins in the mammary tissue of vanadium-treated animals. Further, MCF7 cells were cultured in minimal essential medium and were treated with 100, 175 and 250 lM of vanadium (ammonium monovanadate) for 36 hr. Exposure of MCF7 cells to vanadium led to induction of apoptosis in a dose-dependent manner. It was found further that vanadium treatment brought about a prominent cell cycle arrest and chromosomal condensation, leading to apoptosis (42.62%, p < 0.05). Results of both the in vivo and in vitro study demonstrate that vanadium has the potential to be developed into an anti-breast cancer drug in the near future. ' 2006 Wiley-Liss, Inc.

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Induction of COX-2 protein expression by vanadate in A549 human lung carcinoma cell line through EGF receptor and p38 MAPK-mediated pathway

Cited by 57 publications

References 49 publications

Biological effects of a complex of vanadium(V) with salicylaldehyde semicarbazone in osteoblasts in culture: Mechanism of action

Biological effects of a complex of vanadium(V) with salicylaldehyde semicarbazone in osteoblasts in culture: Mechanism of action

Acrolein Induces Cyclooxygenase-2 and Prostaglandin Production in Human Umbilical Vein Endothelial Cells

Suppression of cell proliferation, induction of apoptosis and cell cycle arrest: Chemopreventive activity of vanadium in vivo and in vitro

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