دورية أكاديمية
4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone promoted gastric cancer growth through prostaglandin E receptor (EP2 and EP4) in vivo and in vitro
| العنوان: | 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone promoted gastric cancer growth through prostaglandin E receptor (EP2 and EP4) in vivo and in vitro |
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| المؤلفون: | Cho, CH, Jin, HC, Sung, JJY, Chu, KM, Leung, WK, Ng, EKO, Shin, VY |
| بيانات النشر: | //www.blackwellpublishing.com/journals/CAS Japan |
| سنة النشر: | 2011 |
| المجموعة: | University of Hong Kong: HKU Scholars Hub |
| مصطلحات موضوعية: | Stomach Neoplasms - chemically induced - metabolism, Receptors, Prostaglandin E, EP4 Subtype - metabolism, EP2 Subtype - metabolism, Nitrosamines - toxicity, Carcinogens - toxicity |
| الوصف: | Prostaglandin E (EP) receptor is positively related with COX-2, which is involved in cancer biology. A mechanistic study on how 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) promotes gastric carcinogenesis is lacking. Recently, we found that nicotine promoted tumor growth through upregulation of the COX-2/prostaglandin E 2 pathway. This extended our study on the involvement of EP receptors in gastric carcinogenesis. Both in vitro and in vivo studies showed that NNK promoted cancer cell growth with concomitant EP2 and EP4 upregulation. We found that NNK stimulated vascular endothelial growth factor (VEGF) and angiogenesis, but suppressed apoptosis by increasing Bcl2 and decreasing caspase-3 expressions. Both EP2 and EP4 siRNA significantly impaired these tumorigenic actions of NNK in xenograft tumor. Cell cycle analysis showed that NNK increased S phase entry with increased cyclin D1 and the associated cyclin-dependent kinase 4/6, and downregulation of p21 and p27. The p38 phosphorylation was EP2/4-dependent, and SB203580 (p38 inhibitor) suppressed NNK-induced prostaglandin E 2, VEGF, and cell proliferation. Antagonists of EP2 or EP4 abolished the elevated VEGF and VEGF receptor-2. These data strongly indicate that EP2/4 are important for NNK-promoted gastric carcinogenesis, thus providing a framework for future evaluation of EP antagonist(s) as anticancer drugs for smokers. © 2011 Japanese Cancer Association. ; link_to_subscribed_fulltext |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| ردمك: | 978-0-00-289630-6 0-00-289630-3 |
| تدمد: | 1347-9032 |
| العلاقة: | Cancer Science; http://www.scopus.com/mlt/select.url?eid=2-s2.0-79954871936&selection=ref&src=s&origin=recordpageTest; Cancer Science, 2011, v. 102 n. 5, p. 926-933; 933; 199104; 184334; WOS:000289630300003; http://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1347-9032&volume=102&issue=5&spage=926&epage=933&date=2011&atitle=4Test-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone+promoted+gastric+cancer+growth+through+prostaglandin+E+receptor+(EP2+and+EP4)+in+vivo+and+in+vitro; eid_2-s2.0-79954871936; 926; http://hdl.handle.net/10722/133654Test; 102 |
| DOI: | 10.1111/j.1349-7006.2011.01885.x |
| الإتاحة: | https://doi.org/10.1111/j.1349-7006.2011.01885.xTest http://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1347-9032&volume=102&issue=5&spage=926&epage=933&date=2011&atitle=4Test-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone+promoted+gastric+cancer+growth+through+prostaglandin+E+receptor+(EP2+and+EP4)+in+vivo+and+in+vitro http://hdl.handle.net/10722/133654Test |
| حقوق: | The definitive version is available at onlinelibrary.wiley.com |
| رقم الانضمام: | edsbas.6E3C871E |
| قاعدة البيانات: | BASE |
Full Text Finder | ردمك: | 9780002896306 0002896303 |
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| تدمد: | 13479032 |
| DOI: | 10.1111/j.1349-7006.2011.01885.x |