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Article: Rab25 is a tumor suppressor gene with antiangiogenic and anti-invasive activities in esophageal squamous cell carcinoma

TitleRab25 is a tumor suppressor gene with antiangiogenic and anti-invasive activities in esophageal squamous cell carcinoma
Authors
Issue Date2012
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Cancer Research, 2012, v. 72 n. 22, p. 6024-6035 How to Cite?
AbstractEsophageal squamous cell carcinoma (ESCC), the major histologic subtype of esophageal cancer, is a devastating disease characterized by distinctly high incidences and mortality rates. However, there remains limited understanding of molecular events leading to development and progression of the disease, which are of paramount importance to defining biomarkers for diagnosis, prognosis, and personalized treatment. By high-throughout transcriptome sequence profiling of nontumor and ESCC clinical samples, we identified a subset of significantly differentially expressed genes involved in integrin signaling. The Rab25 gene implicated in endocytic recycling of integrins was the only gene in this group significantly downregulated, and its downregulation was confirmed as a frequent event in a second larger cohort of ESCC tumor specimens by quantitative real-time PCR and immunohistochemical analyses. Reduced expression of Rab25 correlated with decreased overall survival and was also documented in ESCC cell lines compared with pooled normal tissues. Demethylation treatment and bisulfite genomic sequencing analyses revealed that downregulation of Rab25 expression in both ESCC cell lines and clinical samples was associated with promoter hypermethylation. Functional studies using lentiviral-based overexpression and suppression systems lent direct support of Rab25 to function as an important tumor suppressor with both anti-invasive and -angiogenic abilities, through a deregulated FAK–Raf–MEK1/2–ERK signaling pathway. Further characterization of Rab25 may provide a prognostic biomarker for ESCC outcome prediction and a novel therapeutic target in ESCC treatment.
Persistent Identifierhttp://hdl.handle.net/10722/184488
ISSN
2017 Impact Factor: 9.13
2015 SCImago Journal Rankings: 5.372
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorTong, M-
dc.contributor.authorChan, KW-
dc.contributor.authorBao, JYJ-
dc.contributor.authorWong, KY-
dc.contributor.authorChen, J-
dc.contributor.authorKwan, PS-
dc.contributor.authorTang, KH-
dc.contributor.authorFu, L-
dc.contributor.authorQin, YR-
dc.contributor.authorLok, S-
dc.contributor.authorGuan, X-
dc.contributor.authorMa, S-
dc.date.accessioned2013-07-15T09:50:25Z-
dc.date.available2013-07-15T09:50:25Z-
dc.date.issued2012-
dc.identifier.citationCancer Research, 2012, v. 72 n. 22, p. 6024-6035-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/184488-
dc.description.abstractEsophageal squamous cell carcinoma (ESCC), the major histologic subtype of esophageal cancer, is a devastating disease characterized by distinctly high incidences and mortality rates. However, there remains limited understanding of molecular events leading to development and progression of the disease, which are of paramount importance to defining biomarkers for diagnosis, prognosis, and personalized treatment. By high-throughout transcriptome sequence profiling of nontumor and ESCC clinical samples, we identified a subset of significantly differentially expressed genes involved in integrin signaling. The Rab25 gene implicated in endocytic recycling of integrins was the only gene in this group significantly downregulated, and its downregulation was confirmed as a frequent event in a second larger cohort of ESCC tumor specimens by quantitative real-time PCR and immunohistochemical analyses. Reduced expression of Rab25 correlated with decreased overall survival and was also documented in ESCC cell lines compared with pooled normal tissues. Demethylation treatment and bisulfite genomic sequencing analyses revealed that downregulation of Rab25 expression in both ESCC cell lines and clinical samples was associated with promoter hypermethylation. Functional studies using lentiviral-based overexpression and suppression systems lent direct support of Rab25 to function as an important tumor suppressor with both anti-invasive and -angiogenic abilities, through a deregulated FAK–Raf–MEK1/2–ERK signaling pathway. Further characterization of Rab25 may provide a prognostic biomarker for ESCC outcome prediction and a novel therapeutic target in ESCC treatment.-
dc.languageeng-
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/-
dc.relation.ispartofCancer Research-
dc.titleRab25 is a tumor suppressor gene with antiangiogenic and anti-invasive activities in esophageal squamous cell carcinoma-
dc.typeArticle-
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0008-5472&volume=72&spage=6024&epage=6035&date=2012&atitle=Rab25+is+a+tumor+suppressor+gene+with+anti-angiogenic+and+anti-invasive+activities+in+esophageal+squamous+cell+carcinomaen_US
dc.identifier.emailTong, M: caroltm@hku.hk-
dc.identifier.emailChan, KW: hrmtckw@hku.hk-
dc.identifier.emailBao, JYJ: baoyj@hku.hk-
dc.identifier.emailWong, KY: kywonga@hkucc.hku.hk-
dc.identifier.emailKwan, PS: kwanps@hku.hk-
dc.identifier.emailFu, L: gracefu@graduate.hku.hk-
dc.identifier.emailLok, S: silok@genome.hku.hk-
dc.identifier.emailGuan, X: xyguan@hkucc.hku.hk-
dc.identifier.emailMa, S: stefma@hku.hk-
dc.identifier.authorityTong, M=rp02568-
dc.identifier.authorityChan, KW=rp00330-
dc.identifier.authorityFu, L=rp01435-
dc.identifier.authorityLok, S=rp00271-
dc.identifier.authorityGuan, X=rp00454-
dc.identifier.authorityMa, S=rp00506-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1158/0008-5472.CAN-12-1269-
dc.identifier.pmid22991305-
dc.identifier.scopuseid_2-s2.0-84869228632-
dc.identifier.hkuros215084-
dc.identifier.volume72-
dc.identifier.issue22-
dc.identifier.spage6024-
dc.identifier.epage6035-
dc.identifier.isiWOS:000311141300037-
dc.publisher.placeUnited States-

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