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Article: Effect of celecoxib on E-cadherin, VEGF, microvessel density and apoptosis in gastric cancer

TitleEffect of celecoxib on E-cadherin, VEGF, microvessel density and apoptosis in gastric cancer
Authors
KeywordsAngiogenesis
Apoptosis
Chemoprevention
COX-2 inhibitor
Gastric cancer
Issue Date2007
PublisherLandes Bioscience. The Journal's web site is located at http://www.landesbioscience.com/journals/cbt/index.php
Citation
Cancer Biology And Therapy, 2007, v. 6 n. 2, p. 269-275 How to Cite?
AbstractCyclooxygenase-2 (COX-2) plays a crucial role in the development and invasion of gastric cancer. COX-2 inhibitors have been shown to be chemopreventive against gastrointestinal cancers. In vitro studies have suggested that the mechanisms may be related to induction of apoptosis and inhibition of angiogenesis. COX-2 may also have impact on E-cadherin. In our study we investigate the effect of Celecoxib on expression of E-cadherin and serum soluble E-cadherin, as well as on apoptosis and angiogenesis in patients with gastric cancer. Fifty nine gastric cancer patients were randomly divided into two groups: Surgery group (n = 22), in which patients underwent surgical resection after diagnosis, and Celecoxib + Surgery group (n = 37), in which patients received oral Celecoxib 200 mg twice daily for 7 days before curative resection. Twenty healthy subjects (Healthy controls) were recruited as normal controls. After curative resection, COX-2, E-cadherin, VEGF, and MVD were detected by immunohistochemistry. Serum soluble E-cadherin was quantitatively measured using a commercially available enzyme-linked immunosorbent assay kit. Apoptosis was determined by TUNEL assay. Significantly decreased expression of COX-2, increased E-cadherin and apoptosis, decreased VEGF and MVD were observed in gastric cancer tissues from patients receiving Celecoxib compared to Surgery group. Compared to Healthy controls, the serum soluble E-cadherin levels were higher in gastric cancer patients which were decreased by Celecoxib. This in vivo study demonstrated that Celecoxib induces apoptosis and inhibit angiogenesis of gastric cancer. Its impact on E-cadherin may suggest that this agent may suppress the invasion of advanced gastric cancer. ©2007 Landes Bioscience.
Persistent Identifierhttp://hdl.handle.net/10722/76790
ISSN
2015 Impact Factor: 2.921
2015 SCImago Journal Rankings: 1.297
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhou, Yen_HK
dc.contributor.authorRan, Jen_HK
dc.contributor.authorTang, Cen_HK
dc.contributor.authorWu, Jen_HK
dc.contributor.authorHonghua, Len_HK
dc.contributor.authorXingwen, Len_HK
dc.contributor.authorNing, Cen_HK
dc.contributor.authorQiao, Len_HK
dc.date.accessioned2010-09-06T07:24:56Z-
dc.date.available2010-09-06T07:24:56Z-
dc.date.issued2007en_HK
dc.identifier.citationCancer Biology And Therapy, 2007, v. 6 n. 2, p. 269-275en_HK
dc.identifier.issn1538-4047en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76790-
dc.description.abstractCyclooxygenase-2 (COX-2) plays a crucial role in the development and invasion of gastric cancer. COX-2 inhibitors have been shown to be chemopreventive against gastrointestinal cancers. In vitro studies have suggested that the mechanisms may be related to induction of apoptosis and inhibition of angiogenesis. COX-2 may also have impact on E-cadherin. In our study we investigate the effect of Celecoxib on expression of E-cadherin and serum soluble E-cadherin, as well as on apoptosis and angiogenesis in patients with gastric cancer. Fifty nine gastric cancer patients were randomly divided into two groups: Surgery group (n = 22), in which patients underwent surgical resection after diagnosis, and Celecoxib + Surgery group (n = 37), in which patients received oral Celecoxib 200 mg twice daily for 7 days before curative resection. Twenty healthy subjects (Healthy controls) were recruited as normal controls. After curative resection, COX-2, E-cadherin, VEGF, and MVD were detected by immunohistochemistry. Serum soluble E-cadherin was quantitatively measured using a commercially available enzyme-linked immunosorbent assay kit. Apoptosis was determined by TUNEL assay. Significantly decreased expression of COX-2, increased E-cadherin and apoptosis, decreased VEGF and MVD were observed in gastric cancer tissues from patients receiving Celecoxib compared to Surgery group. Compared to Healthy controls, the serum soluble E-cadherin levels were higher in gastric cancer patients which were decreased by Celecoxib. This in vivo study demonstrated that Celecoxib induces apoptosis and inhibit angiogenesis of gastric cancer. Its impact on E-cadherin may suggest that this agent may suppress the invasion of advanced gastric cancer. ©2007 Landes Bioscience.en_HK
dc.languageengen_HK
dc.publisherLandes Bioscience. The Journal's web site is located at http://www.landesbioscience.com/journals/cbt/index.phpen_HK
dc.relation.ispartofCancer Biology and Therapyen_HK
dc.subjectAngiogenesisen_HK
dc.subjectApoptosisen_HK
dc.subjectChemopreventionen_HK
dc.subjectCOX-2 inhibitoren_HK
dc.subjectGastric canceren_HK
dc.titleEffect of celecoxib on E-cadherin, VEGF, microvessel density and apoptosis in gastric canceren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1538-4047&volume=26&spage=269&epage=75&date=2007&atitle=Effect+of+Celecoxib+on+E-cadherin,+VEGF,+microvessel+density,+and+apoptosis+in+gastric+canceren_HK
dc.identifier.emailQiao, L: lq8688@hotmail.comen_HK
dc.identifier.authorityQiao, L=rp00513en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid17224647-
dc.identifier.scopuseid_2-s2.0-34247365049en_HK
dc.identifier.hkuros132100en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34247365049&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume6en_HK
dc.identifier.issue2en_HK
dc.identifier.spage269en_HK
dc.identifier.epage275en_HK
dc.identifier.isiWOS:000245851800034-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridZhou, Y=7405364644en_HK
dc.identifier.scopusauthoridRan, J=16240029600en_HK
dc.identifier.scopusauthoridTang, C=19639622400en_HK
dc.identifier.scopusauthoridWu, J=8220448800en_HK
dc.identifier.scopusauthoridHonghua, L=16238755100en_HK
dc.identifier.scopusauthoridXingwen, L=26533627900en_HK
dc.identifier.scopusauthoridNing, C=16239051100en_HK
dc.identifier.scopusauthoridQiao, L=7202151719en_HK

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