The Effects of Cyclooxygenase2–ProstaglandinE2 Pathway on <i>Helicobacter pylori</i>‐Induced Urokinase‐Type Plasminogen Activator System in the Gastric Cancer Cells

Iwamoto, Junichi; Mizokami, Yuji; Takahashi, Kimiko; Matsuoka, Takeshi; Matsuzaki, Yasushi

doi:10.1111/j.1523-5378.2008.00597.x

Cited by 26 publications

(23 citation statements)

References 37 publications

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“…Furthermore, COX2 can induce angiogenesis via VEGF and b Wbroblast growth factor (bFGF) expression, and increases the metastatic potential by up-regulation of uPA and matrixmetallo-proteinase 2 (MMP2). These changes result in an increased tumourigenic potential and supports the hypothesis that COX2 over-expression plays a key role in the cancer transformation process (Iwamoto et al 2008).…”

Section: Cox Inhibitorssupporting

confidence: 79%

Gastric cancer in the era of molecularly targeted agents: current drug development strategies

Arkenau

2009

J Cancer Res Clin Oncol

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Gastric cancer is the second most common cause of cancer death worldwide with approximately one million cases diagnosed annually. Despite considerable improvements in surgical techniques, innovations in clinical diagnostics and the development of new chemotherapy regimens, the clinical outcome for patients with advanced gastric cancer and cancer of the GEJ is generally poor with 5-year survival rates ranging between 5 and 15%. The understanding of cancer relevant events has resulted in new therapeutic strategies, particularly in developing of new molecular targeted agents. These agents have the ability to target a variety of cancer relevant receptors and downstream pathways including the epidermal growth factor receptor (EGFR), the vascular endothelial growth factor receptor (VEGFR), the insulin-like growth factor receptor (IGFR), the c-Met pathway, cell-cycle pathways, and down-stream signalling pathways such as the Akt-PI3k-mTOR pathway. In the era of new molecularly targeted agents this review focuses on recent developments of targeting relevant pathways involved in gastric cancer and cancer of the GEJ.

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Section: Cox Inhibitorssupporting

confidence: 79%

Gastric cancer in the era of molecularly targeted agents: current drug development strategies

Arkenau

2009

J Cancer Res Clin Oncol

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“…Chronic atrophic gastritis caused by H. pylori activates synthesis of growth factors, cytokines, and gastrin leading to elevated COX-2 expression [19]. Furthermore, CagA-positive H. pylori infection associates with COX-2 expression in human gastric cancer [20], and in gastric cancer cells H. pylori exposure elevates COX-2 expression [21]. H. pylori may thus play an important role in induction of COX-2 synthesis during chronic gastritis that is a precancerous condition for gastric cancer.…”

Section: Cox-in Human Gastric Carcinogenesismentioning

confidence: 99%

Cyclooxygenase-2 and Gastric Cancer

Thiel

Mrena

Ristimäki

2011

Cancer Metastasis Rev

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Gastric cancer remains a leading cause of cancer-related deaths worldwide, although its incidence has been steadily declining during recent decades. Expression of cyclooxygenase-2 (COX-2) is elevated in gastric carcinomas and in their precursor lesions. COX-2 expression associates with reduced survival in gastric cancer patients, and it has also been shown to be an independent factor of poor prognosis. Several molecular mechanisms are involved in the regulation of COX-2 expression in gastric cancer cell lines, including signal transduction pathways activated by Helicobacter pylori. In gastric tumor models in vivo the role of COX-2 seems to be predominantly to facilitate tumor promotion and growth.

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“…pylori has been related to induction of uPAR. Several in vitro studies have found that the expression of uPAR is upregulated in cancer and gastric epithelial cell lines when co-cultured with H. pylori (Guillemin, Salama, Tompkins, & Falkow, 2002;Sepulveda et al, 2002;El-Etr, Mueller, Tompkins, Falkow, & Merrell, 2004;Iwamoto et al, 2005;Kim et al, 2005;Kim et al, 2007;Iwamoto, Mizokami, Takahashi, Matsuoka, & Matsuzaki, 2008). This phenomenon has also been documented in vivo, specifically in non-neoplastic tissue (adjacent to the tumor growth) obtained from GC patients (Alpízar-Alpízar et al, 2010), as well as in gastric biopsies from patients that have no cancer but are infected with the bacterium (Kenny et al, 2008).…”

Section: Plasminogen Activation System and Helicobacter Pylorimentioning

confidence: 83%

La importancia del sistema activador de plasminógeno en la patogénesis y progresión del cáncer gástrico

Alpízar‐Alpízar

Malespín-Bendaña

Une

et al. 2017

RBT

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Gastric cancer is ranked as the third death-causing cancer and one of the most incident malignancies worldwide. Although Helicobacter pylori is the most well-established risk factor for the development of this neoplasm, most of the infected individuals do not develop gastric cancer. Two of the main challenges faced by the world's scientific community in the combat against gastric cancer are the unraveling of its pathogenesis and the identification of novel ways to bring down the mortality. Malignant cell invasion of the non-neoplastic adjacent tissue and metastasis are pivotal events during cancer development and progression. Both processes are facilitated by proteases capable of degrading components of the extracellular matrix, some of which have been associated to clinic-pathological aspects of the disease. Recent studies have suggested the possible connection between H. pylori and the expression of some of these proteases in gastric mucosa. This review summarizes the current knowledge about epidemiological, clinical and biological aspects of gastric cancer; it also discusses the main findings about the involvement of the plasminogen activation system in the development and progression of this disease, as well as its potential repercussions in the clinical setting. Rev. Biol. Trop. 66(1): 28-47. Epub 2018 March 01.

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The Effects of Cyclooxygenase2–ProstaglandinE2 Pathway on Helicobacter pylori‐Induced Urokinase‐Type Plasminogen Activator System in the Gastric Cancer Cells

Abstract: Our results indicated that COX2-PGE2 pathway may be involved in H. pylori-associated uPA and uPAR induction, and that COX-2 inhibitor or EP2 receptor antagonist may inhibit angiogenesis and tumor invasion via suppression of the uPA system.

Cited by 26 publications

References 37 publications

Gastric cancer in the era of molecularly targeted agents: current drug development strategies

Gastric cancer in the era of molecularly targeted agents: current drug development strategies

Cyclooxygenase-2 and Gastric Cancer

La importancia del sistema activador de plasminógeno en la patogénesis y progresión del cáncer gástrico

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