<i>Helicobacter pylori</i>promote gastric cancer cells invasion through a NF-kB and COX-2-mediated pathway

Wu, Chun Ying; Wang, Chau Jong; Tseng, Chi Chuan; Chen, Hsiao Ping; Wu, Ming Shing; Lin, Jaw Town; Inoue, H.; Chen, Gran Hum

doi:10.3748/wjg.v11.i21.3197

Cited by 87 publications

(67 citation statements)

References 27 publications

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“…Therefore, it is suggested that the stimulatory action of nicotine on invasiveness (migration of cancer cells) and angiogenesis (mobility of endothelial cells) are dependent on COX-2 activity and the angiogenic action of VEGF. This phenomenon is in accord with other study that inhibitor of COX-2 markedly reduces Helicobacter pylori -promoted gastric cancer cell invasion, concomitant with down-regulation of MMP-9 and VEGF protein expressions (39).…”

Section: Discussionsupporting

confidence: 93%

Nicotine Induces Cyclooxygenase-2 and Vascular Endothelial Growth Factor Receptor-2 in Association with Tumor-Associated Invasion and Angiogenesis in Gastric Cancer

Shin¹,

Wu²,

Chu³

et al. 2005

Molecular Cancer Research

103

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Blockade of angiogenesis is a promising strategy to suppress tumor growth, invasion, and metastasis. Vascular endothelial growth factor (VEGF), which binds to tyrosine kinase receptors [VEGF receptors (VEGFR) 1 and 2], is the mediator of angiogenesis and mitogen for endothelial cells. Cyclooxygenase-2 (COX-2) plays an important role in the promoting action of nicotine on gastric cancer growth. However, the action of nicotine and the relationship between COX-2 and VEGF/VEGFR system in tumorigenesis remain undefined. In this study, the effects of nicotine in tumor angiogenesis, invasiveness, and metastasis were studied with sponge implantation and Matrigel membrane models. Nicotine (200 Mg/mL) stimulated gastric cancer cell proliferation, which was blocked by SC-236 (a highly selective COX-2 inhibitor) and CBO-P11 (a VEGFR inhibitor). This was associated with decreased VEGF levels as well as VEGFR-2 but not VEGFR-1 expression. Topical injection of nicotine enhanced tumor-associated vascularization, with a concomitant increase in VEGF levels in sponge implants. Again, application of SC-236 (2 mg/kg) and CBO-P11 (0.4 mg/kg) partially attenuated vascularization by f30%. Furthermore, nicotine enhanced tumor cell invasion through the Matrigel membrane by 4-fold and promoted migration of human umbilical vein endothelial cells in a cocultured system with gastric cancer cells. The activity of matrix metalloproteinases 2 and 9 and protein expressions of plasminogen activators (urokinase-type plasminogen activator and its receptor), which are the indicators of invasion and migration processes, were increased by nicotine but blocked by COX-2 and VEGFR inhibitors. Taken together, our results reveal that the promoting action of nicotine on angiogenesis, tumor invasion, and metastasis is COX-2/VEGF/VEGFR dependent. (Mol Cancer Res 2005;3(11):607 -15)

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Section: Discussionsupporting

confidence: 93%

Nicotine Induces Cyclooxygenase-2 and Vascular Endothelial Growth Factor Receptor-2 in Association with Tumor-Associated Invasion and Angiogenesis in Gastric Cancer

Shin¹,

Wu²,

Chu³

et al. 2005

Molecular Cancer Research

103

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“…This process is carried out by MMPs. A basic component of the extracellular matrix is type IV collagen that is degraded by MMP-2 and MMP-9 [Wu et al, 2005]. These results are consistent with previous reports that SFN suppresses metastasis through the COX-2/MMP-2/9 pathway [Shan et al, 2013].…”

Section: Discussionsupporting

confidence: 92%

Sulforaphane, a Chemopreventive Compound, Inhibits Cyclooxygenase-2 and Microsomal Prostaglandin E Synthase-1 Expression in Human HT-29 Colon Cancer Cells

Tafakh

Saidijam

Ranjbarnejad

et al. 2018

Cells Tissues Organs

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Background: A high expression of prostaglandin E2 (PGE2) is found in colorectal cancer. Therefore, blocking of PGE2 generation has been identified as a promising approach for anticancer therapy. Sulforaphane (SFN), an isothiocyanate derived from glucosinolate, is used as the antioxidant and anticancer agents. Methods: HT-29 cells were treated with various concentrations of SFN and compared to untreated cells for the expression of microsomal prostaglandin E synthase-1 (mPGES-1), cyclooxygenase 2 (COX-2), hypoxia-inducible factor-1 (HIF-1), C-X-C chemokine receptor type 4 (CXCR4), vascular endothelial growth factor (VEGF), and matrix metalloproteinase (MMP)-2 and MMP-9 at the mRNA level. The PGE2 level was measured by ELISA assay. Apoptosis was evaluated by the proportion of sub-G1 cells. The activity of caspase-3 was determined using an enzymatic assay. HT-29 cell migration was assessed using a scratch test. Results: SFN preconditioning decreased the expression of COX-2, mPGES-1, HIF-1, VEGF, CXCR4, MMP-2, and MMP-9. An apoptotic effect of SFN was preceded by the activation of caspase-3 as well as accumulation of cells in the sub-G1 phase of the cell cycle. SFN decreased PGE2 generation and inhibited the in vitro motility/wound-healing activity of HT-29 cells. Conclusions: SFN anticancer effects are associated with antiproliferative, antiangiogenic, and antimetastatic activities arising from the downregulation of the COX-2/ mPGES-1 axis.

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“…Several studies have suggested COX-2 as an important factor in gastric carcinoma associated with Helicobacter pylori infection (7,53), and its roles in the diseases caused by obligate intracellular bacteria of Chlamydia species and pathogenic spirochetes of Borrelia species have begun to be elucidated only recently (1,18,28). Although the status of COX isozymes in EC infected with typhus rickettsiae is currently under investigation, evidence derived from the presented data and earlier observations (48,50) suggest significant increases in the production of the major endothelial prostaglandins PGE 2 and PGI 2 during infection and implicate COX-2 and its reaction metabolites as having an integral role in the pathophysiology of rickettsial diseases.…”

Section: Discussionmentioning

confidence: 99%

Infection of Human Endothelial Cells with Spotted Fever Group Rickettsiae Stimulates Cyclooxygenase 2 Expression and Release of Vasoactive Prostaglandins

Rydkina¹,

Sahni²,

Baggs

et al. 2006

Infect Immun

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Rickettsiae, a diverse group of obligately intracellular gram-negative bacteria, include etiologic agents of the spotted fever and typhus groups of diseases. Rocky Mountain spotted fever and boutonneuse fever, due to Rickettsia rickettsii and R. conorii, respectively, are characterized by widespread infection of the vascular endothelium, microvascular injury, and vasculitis. Cultured human endothelial cells (EC) are highly susceptible to infection and respond by altering the expression of adhesion molecules, regulatory cytokines, and the antioxidant enzyme heme oxygenase (HO). In the vasculature, HO regulates the cyclooxygenase (COX) enzymes, among which the inducible isozyme COX-2 facilitates the synthesis of prostaglandins (PGs). Using in vitro and ex vivo models of infection, we demonstrate here that R. rickettsii infection of human EC causes robust induction of COX-2 mRNA and protein expression but has no apparent effect on the constitutive COX-1 isoform. Cells infected with viable rickettsiae consistently displayed significantly increased secretion of 6-keto-PGF 1␣ and PGE 2 . R. rickettsii-induced COX-2 was sensitive to inhibitors of de novo transcription and the pyridinylimidazole-based compound SB 203580, suggesting that this transcriptional host cell response involves signaling through p38 mitogen-activated protein kinase. PG production by infected cells was abrogated by NS 398 (a selective COX-2 inhibitor) and indomethacin (a pan-COX inhibitor). Immunohistochemical staining of sections of infected umbilical cords and corresponding uninfected controls revealed comparatively more intense and abundant staining for COX-2 in infected endothelia. Induction of the endothelial COX-2 system and the resultant enhanced release of vasoactive PGs may contribute to the regulation of inflammatory responses and vascular permeability changes during spotted fever rickettsioses.Pathogenic species of the genus Rickettsia include gramnegative bacteria capable of causing mild to severe diseases in humans. Spotted fever group (SFG) organisms, which represent one of the two major groups of rickettsiae, are found globally in their characteristic arthropod vectors and are often classified to reflect the location of their predominant geographic distribution, for example, Rickettsia sibirica and R. australis, or the resultant human disease, such as Rocky Mountain spotted fever and Mediterranean spotted fever, caused by R. rickettsii and R. conorii, respectively (27, 47). Rocky Mountain spotted fever is a life-threatening illness and can be fatal in children, the elderly, and immunodeficient individuals if there is a lack of early detection and timely intervention with suitable antibiotic therapy. Yet another recently realized and alarming epidemiologic aspect of this disease is that tick-to-human transmission can occur not only through the previously identified principal vectors of Dermacentor species, but also through the more commonly distributed brown dog tick, Rhipicephalus sanguineus, suggesting the capability of this obliga...

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Helicobacter pyloripromote gastric cancer cells invasion through a NF-kB and COX-2-mediated pathway

Cited by 87 publications

References 27 publications

Nicotine Induces Cyclooxygenase-2 and Vascular Endothelial Growth Factor Receptor-2 in Association with Tumor-Associated Invasion and Angiogenesis in Gastric Cancer

Nicotine Induces Cyclooxygenase-2 and Vascular Endothelial Growth Factor Receptor-2 in Association with Tumor-Associated Invasion and Angiogenesis in Gastric Cancer

Sulforaphane, a Chemopreventive Compound, Inhibits Cyclooxygenase-2 and Microsomal Prostaglandin E Synthase-1 Expression in Human HT-29 Colon Cancer Cells

Infection of Human Endothelial Cells with Spotted Fever Group Rickettsiae Stimulates Cyclooxygenase 2 Expression and Release of Vasoactive Prostaglandins

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