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Journal of Environmental Pathology, Toxicology and Oncology

Published 4 issues per year

ISSN Print: 0731-8898

ISSN Online: 2162-6537

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 2.4 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.8 The Immediacy Index is the average number of times an article is cited in the year it is published. The journal Immediacy Index indicates how quickly articles in a journal are cited. Immediacy Index: 0.5 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00049 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.59 SJR: 0.429 SNIP: 0.507 CiteScore™:: 3.9 H-Index: 49

Indexed in

Oxidant-Sensitive Transcription Factor and Cyclooxygenase-2 by Helicobacter pylori Stimulation in Human Gastric Cancer Cells

Volume 21, Issue 2, 2002, 9 pages
DOI: 10.1615/JEnvironPatholToxicolOncol.v21.i2.50
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ABSTRACT

Helicobacter pylori (H. pylori) infection might activate nuclear factor-kB (NF-kB), an oxidant-sensitive transcription regulator of inducible expression of inflammatory genes such as cyclooxygenase-2 (COX-2). We studied the role of NF-kB on expression of COX-2 in H. pylori-stimulated gastric cancer cell lines by using antioxidants, glutathione (GSH), and N-acetylcysteine (NAC) as well as an NF-kB inhibitor, pyrrolidine dithiocarbamate (PDTC). Gastric adenocarcinoma cell lines derived from Caucasian (AGS) cells and Korean (SNU-484) cells were used to study the role of NF-kB on COX-2 expression by H. pylori. They were treated with GSH, NAC, or PDTC in the presence of H. pylori. mRNA expression and protein level for COX-2 were determined by Northern blot and RT-PCR analysis as well as Western blot analysis. NF-kB activation was examined by electrophoretic mobility shift assay. As a result, H. pylori induced a time-dependent expression of mRNA and protein for COX-2 via activation of NF-kB, which was inhibited by GSH, NAC, and PDTC in the cells. In conclusion, oxidant-sensitive transcription factor NF-kB may play a novel role in expression of COX-2 by H. pylori stimulation in gastric cancer cells.

CITED BY
  1. Gisbert Javier P., María Pajares José, Ciclooxigenasa 2 (COX-2), Helicobacter pylori y cáncer gástrico, Medicina Clínica, 120, 5, 2003. Crossref

  2. Yu Y.Y., Li Q., Zhu Z.G., NF-κB as a molecular target in adjuvant therapy of gastrointestinal carcinomas, European Journal of Surgical Oncology (EJSO), 31, 4, 2005. Crossref

  3. Yang Gui-Fang, Expression of nuclear factor-kappa B and target genes in gastric precancerous lesions and adenocarcinoma: Association withHelicobactor pyloricagA (+) infection, World Journal of Gastroenterology, 10, 4, 2004. Crossref

  4. Wu James T., Identification of Risk Factors for Early Neoplasm, in Cancer Diagnostics, 2004. Crossref

  5. Jiang Jun-Yan, Liu Dai-Jiang, Liu Mao-Xia, The protective effect of NF-κB signaling pathway inhibitor PDTC on mice with chronic atrophic gastritis, Scandinavian Journal of Gastroenterology, 56, 10, 2021. Crossref

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