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Article: Human beta-defensin-3 (hBD-3) upregulated by LPS via epidermal growth factor receptor (EGFR) signaling pathways to enhance lymphatic invasion of oral squamous cell carcinoma

TitleHuman beta-defensin-3 (hBD-3) upregulated by LPS via epidermal growth factor receptor (EGFR) signaling pathways to enhance lymphatic invasion of oral squamous cell carcinoma
Authors
Issue Date2011
PublisherMosby, Inc. The Journal's web site is located at http://www.elsevier.com/locate/tripleo
Citation
Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and Endodontology, 2011, v. 112 n. 5, p. 616-625 How to Cite?
AbstractOBJECTIVE: In this study, the hypothesis that hBD-3 is upregulated by LPS via epidermal growth factor receptor (EGFR) signaling pathways to enhance metastasis in oral squamous cell carcinoma (OSCC) was tested. STUDY DESIGN: hBD-3 expression in human tissue specimens was evaluated by RT-qPCR and immunohistochemical staining. The presence of hBD-3 peptide in the culture supernatants of each type of treated cells was evaluated by enzyme-linked immunosorbent assay. The chemotaxis response to LPS or hBD-3 protein of SCC-25 cells or siRNA-hBD-3 transfected cells were also measured by chemotaxis assay. Paired, 2-tailed Student t test and analysis of variance was used to assess the statistical significance between 2 groups or many groups. RESULTS: hBD-3 is highly expressed and associated with lymphatic invasion of OSCC. hBD-3 expression and EGFR phosphorylation were markedly upregulated when SCC-25 cells were treated with LPS. When SCC-25 cells were preincubated with EGFR inhibitor or TLR4-neutralizing Ab before LPS stimulation, a decrease in the expression of hBD-3 was observed. hBD-3 markedly enhanced cancer metastasis, and the chemotaxis response to LPS of SCC-25 cells was partly blocked by siRNA target hBD-3. CONCLUSION: These findings indicate that hBD-3 is upregulated by LPS via EGFR signaling pathways to enhance lymphatic invasion of OSCC.
Persistent Identifierhttp://hdl.handle.net/10722/154686
ISSN
2011 Impact Factor: 1.457
ISI Accession Number ID
Funding AgencyGrant Number
National Natural Science Foundation of China30973339
Guangdong Natural Science Foundation104518036002006000
foundation of Shenzhen Bureau of Science Technology and InformationJC200903180665A
Guangdong science and technology projects2010B050100007
Funding Information:

This work was supported by the National Natural Science Foundation of China (grant no. 30973339), the Guangdong Natural Science Foundation (grant no. 104518036002006000), and the foundation of Shenzhen Bureau of Science Technology and Information (grant no. JC200903180665A), and the Guangdong science and technology projects (grant no. 2010B050100007).

References

 

DC FieldValueLanguage
dc.contributor.authorYu, Sen_US
dc.contributor.authorWang, Fen_US
dc.contributor.authorTang, Jen_US
dc.contributor.authorHuang, HZen_US
dc.contributor.authorWang, HYen_US
dc.contributor.authorMa, PPen_US
dc.contributor.authorZheng, Len_US
dc.contributor.authorZwahlen, RAen_US
dc.contributor.authorYang, HYen_US
dc.date.accessioned2012-08-08T08:26:54Z-
dc.date.available2012-08-08T08:26:54Z-
dc.date.issued2011en_US
dc.identifier.citationOral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and Endodontology, 2011, v. 112 n. 5, p. 616-625en_US
dc.identifier.issn1079-2104en_US
dc.identifier.urihttp://hdl.handle.net/10722/154686-
dc.description.abstractOBJECTIVE: In this study, the hypothesis that hBD-3 is upregulated by LPS via epidermal growth factor receptor (EGFR) signaling pathways to enhance metastasis in oral squamous cell carcinoma (OSCC) was tested. STUDY DESIGN: hBD-3 expression in human tissue specimens was evaluated by RT-qPCR and immunohistochemical staining. The presence of hBD-3 peptide in the culture supernatants of each type of treated cells was evaluated by enzyme-linked immunosorbent assay. The chemotaxis response to LPS or hBD-3 protein of SCC-25 cells or siRNA-hBD-3 transfected cells were also measured by chemotaxis assay. Paired, 2-tailed Student t test and analysis of variance was used to assess the statistical significance between 2 groups or many groups. RESULTS: hBD-3 is highly expressed and associated with lymphatic invasion of OSCC. hBD-3 expression and EGFR phosphorylation were markedly upregulated when SCC-25 cells were treated with LPS. When SCC-25 cells were preincubated with EGFR inhibitor or TLR4-neutralizing Ab before LPS stimulation, a decrease in the expression of hBD-3 was observed. hBD-3 markedly enhanced cancer metastasis, and the chemotaxis response to LPS of SCC-25 cells was partly blocked by siRNA target hBD-3. CONCLUSION: These findings indicate that hBD-3 is upregulated by LPS via EGFR signaling pathways to enhance lymphatic invasion of OSCC.en_US
dc.languageengen_US
dc.publisherMosby, Inc. The Journal's web site is located at http://www.elsevier.com/locate/tripleoen_US
dc.relation.ispartofOral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and Endodontologyen_US
dc.subject.meshBeta-Defensins - Drug effects - Immunology - Metabolismen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.subject.meshSignal Transduction - Immunology - Physiologyen_US
dc.subject.meshReceptor, Epidermal Growth Factor - Metabolismen_US
dc.subject.meshNeoplasm Invasivenessen_US
dc.subject.meshMouth Neoplasms - Immunology - Pathologyen_US
dc.subject.meshLymphatic Metastasisen_US
dc.subject.meshLymphangiogenesis - Drug Effects - Physiologyen_US
dc.subject.meshLipopolysaccharides - Metabolism - Pharmacologyen_US
dc.subject.meshCarcinoma, Squamous Cell - Immunology - Pathologyen_US
dc.titleHuman beta-defensin-3 (hBD-3) upregulated by LPS via epidermal growth factor receptor (EGFR) signaling pathways to enhance lymphatic invasion of oral squamous cell carcinomaen_US
dc.typeArticleen_US
dc.identifier.emailZheng, L: lwzheng@hku.hken_US
dc.identifier.emailZwahlen, RA: zwahlen@hku.hken_US
dc.identifier.authorityZheng, L=rp01411en_US
dc.identifier.authorityZwahlen, RA=rp00055en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.tripleo.2011.02.053en_US
dc.identifier.pmid22035653-
dc.identifier.scopuseid_2-s2.0-80055085570en_US
dc.identifier.hkuros204636-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80055085570&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume112en_US
dc.identifier.issue5en_US
dc.identifier.spage616en_US
dc.identifier.epage625en_US
dc.identifier.isiWOS:000296565800017-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridHongyu, Y=8924442000en_US
dc.identifier.scopusauthoridZwahlen, RA=7004217269en_US
dc.identifier.scopusauthoridLiwu, Z=54391382700en_US
dc.identifier.scopusauthoridPingping, M=53981843700en_US
dc.identifier.scopusauthoridHaiyan, W=23987094400en_US
dc.identifier.scopusauthoridHongzhang, H=53981290100en_US
dc.identifier.scopusauthoridJing, T=54391130900en_US
dc.identifier.scopusauthoridFeng, W=11241247300en_US
dc.identifier.scopusauthoridShuyi, Yu=54391760400en_US

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