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Article: Targeting NF-κB signaling pathway suppresses tumor growth, angiogenesis, and metastasis of human esophageal cancer

TitleTargeting NF-κB signaling pathway suppresses tumor growth, angiogenesis, and metastasis of human esophageal cancer
Authors
Issue Date2009
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://mct.aacrjournals.org/
Citation
Molecular Cancer Therapeutics, 2009, v. 8 n. 9, p. 2635-2644 How to Cite?
AbstractEsophageal cancer is the eighth most common malignancy, and one of the leading causes of cancer-related deaths worldwide. The overall 5-year survival rate of patients with esophageal cancer remains low at 10% to 40% due to late diagnosis, metastasis, and resistance of the tumor to radiotherapy and chemotherapy. NF-κB is involved in the regulation of cell growth, survival, and motility, but little is known about the role of this signaling pathway in the tumorigenesis of human esophageal squamous cell carcinoma (ESCC), the most common form of esophageal cancer. This study aims to explore the functions of NF-κB in human ESCC progression and to determine whether targeting the NF-κB signaling pathway might be of therapeutic value against ESCC. Our results from human ESCC cell lines and ESCC tissue indicated that NF-κB is constitutively active in ESCC. Exposure of ESCC cells to two NF-κB inhibitors, Bay11-7082 and sulfasalazine, not only reduced cancer cell proliferation, but also induced apoptosis and enhanced sensitivity to chemotherapeutic drugs, 5-fluorouracil, and cisplatin. In addition, Bay11-7082 and sulfasalazine suppressed the migration and invasive potential of ESCC cells. More importantly, the results from tumor xenograft and experimental metastasis models showed that Bay11-7082 had significant antitumor effects on ESCC xenografts in nude mice by promoting apoptosis, and inhibiting proliferation and angiogenesis, as well as reduced the metastasis of ESCC cells to the lungs without significant toxic effects. In summary, our data suggest that NF-κB inhibitors may be potentially useful as therapeutic agents for patients with esophageal cancer. Copyright © 2009 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/67390
ISSN
2015 Impact Factor: 5.579
2015 SCImago Journal Rankings: 3.224
ISI Accession Number ID
Funding AgencyGrant Number
University of Hong Kong Committee on Research and Conference Grants Small Project200807176012
Research Grants Council of the Hong KongHKUST 2/06C
Funding Information:

The University of Hong Kong Committee on Research and Conference Grants Small Project Funding Program project 200807176012 (A.L.M. Cheung), and partly by a Collaborative Research Fund from the Research Grants Council of the Hong Kong Special Administrative Region project HKUST 2/06C.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorLi, Ben_HK
dc.contributor.authorYuk, YLen_HK
dc.contributor.authorSai, WTen_HK
dc.contributor.authorCheung, ALMen_HK
dc.date.accessioned2010-09-06T05:54:43Z-
dc.date.available2010-09-06T05:54:43Z-
dc.date.issued2009en_HK
dc.identifier.citationMolecular Cancer Therapeutics, 2009, v. 8 n. 9, p. 2635-2644en_HK
dc.identifier.issn1535-7163en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67390-
dc.description.abstractEsophageal cancer is the eighth most common malignancy, and one of the leading causes of cancer-related deaths worldwide. The overall 5-year survival rate of patients with esophageal cancer remains low at 10% to 40% due to late diagnosis, metastasis, and resistance of the tumor to radiotherapy and chemotherapy. NF-κB is involved in the regulation of cell growth, survival, and motility, but little is known about the role of this signaling pathway in the tumorigenesis of human esophageal squamous cell carcinoma (ESCC), the most common form of esophageal cancer. This study aims to explore the functions of NF-κB in human ESCC progression and to determine whether targeting the NF-κB signaling pathway might be of therapeutic value against ESCC. Our results from human ESCC cell lines and ESCC tissue indicated that NF-κB is constitutively active in ESCC. Exposure of ESCC cells to two NF-κB inhibitors, Bay11-7082 and sulfasalazine, not only reduced cancer cell proliferation, but also induced apoptosis and enhanced sensitivity to chemotherapeutic drugs, 5-fluorouracil, and cisplatin. In addition, Bay11-7082 and sulfasalazine suppressed the migration and invasive potential of ESCC cells. More importantly, the results from tumor xenograft and experimental metastasis models showed that Bay11-7082 had significant antitumor effects on ESCC xenografts in nude mice by promoting apoptosis, and inhibiting proliferation and angiogenesis, as well as reduced the metastasis of ESCC cells to the lungs without significant toxic effects. In summary, our data suggest that NF-κB inhibitors may be potentially useful as therapeutic agents for patients with esophageal cancer. Copyright © 2009 American Association for Cancer Research.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://mct.aacrjournals.org/en_HK
dc.relation.ispartofMolecular Cancer Therapeuticsen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshEsophageal Neoplasms - blood supply - metabolism - pathology-
dc.subject.meshNF-kappa B - metabolism-
dc.subject.meshNeoplasm Metastasis-
dc.subject.meshNeovascularization, Pathologic-
dc.subject.meshSignal Transduction-
dc.titleTargeting NF-κB signaling pathway suppresses tumor growth, angiogenesis, and metastasis of human esophageal canceren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1535-7163&volume=8&issue=9&spage=2635&epage=2644&date=2009&atitle=Targeting+NF-kB+signaling+pathway+suppresses+tumor+growth,+angiogenesis,+and+metastasis+of+human+esophageal+canceren_HK
dc.identifier.emailCheung, ALM:lmcheung@hkucc.hku.hken_HK
dc.identifier.authorityCheung, ALM=rp00332en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1158/1535-7163.MCT-09-0162en_HK
dc.identifier.pmid19723887en_HK
dc.identifier.scopuseid_2-s2.0-70349501963en_HK
dc.identifier.hkuros167800en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-70349501963&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume8en_HK
dc.identifier.issue9en_HK
dc.identifier.spage2635en_HK
dc.identifier.epage2644en_HK
dc.identifier.eissn1538-8514-
dc.identifier.isiWOS:000269968900016-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectEsophageal Carcinoma Research Center-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.identifier.scopusauthoridLi, B=16138329900en_HK
dc.identifier.scopusauthoridYuk, YL=35186666200en_HK
dc.identifier.scopusauthoridSai, WT=6507617572en_HK
dc.identifier.scopusauthoridCheung, ALM=7401806497en_HK

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