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Article: Identification of retinoic acid-regulated nuclear matrix-associated protein as a novel regulator of gastric cancer
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TitleIdentification of retinoic acid-regulated nuclear matrix-associated protein as a novel regulator of gastric cancer
 
AuthorsLi, J3
Ng, EKO3
Ng, YP2
Wong, CYP3
Yu, J3
Jin, H3
Cheng, VYY4
Go, MYY3
Cheung, PKF3
Ebert, MPA2
Tong, J3
To, KF3
Chan, FKL3
Sung, JJY3
Ip, NY2
Leung, WK1 3
 
KeywordsDTL/RAMP
L2DTL
Oncogene
P21
P53
Tumourigenesis
 
Issue Date2009
 
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjc
 
CitationBritish Journal Of Cancer, 2009, v. 101 n. 4, p. 691-698 [How to Cite?]
DOI: http://dx.doi.org/10.1038/sj.bjc.6605202
 
AbstractBackground: Retinoic acid-regulated nuclear matrix-associated protein (RAMP) is a WD40 repeat-containing protein that is involved in various biological functions, but little is known about its role in human cancer. This study aims to delineate the oncogenic role of RAMP in gastric carcinogenesis.Methods: RAMP expression was examined by real-time quantitative RT-PCR, immunohistochemistry and western blotting. Inhibition of RAMP expression was performed by siRNA-mediated knockdown. The functional effects of RAMP on cell kinetics were measured by cell viability assay, colony formation assay and flow cytometry. Cell lines stably expressing RAMP were established to investigate the oncogenic effects of RAMP in vitro.Results: Ramp was readily expressed in all seven gastric cancer cell lines and was significantly increased in human gastric cancer tissues when compared with their adjacent non-cancerous tissues (P0.001). In keeping with this, expression of RAMP protein was higher in gastric cancer tissues compared with their adjacent non-cancerous tissues, whereas moderate protein expression were noted in intestinal metaplasia. Knockdown of RAMP in gastric cancer cells significantly reduced cell proliferation (P0.01) and soft agar colony formation (P0.001), but induced apoptosis and G 2 /M arrest. In additional, knockdown RAMP induced cell apoptosis is dependent on functional accumulation of p53 and p21 and induction of cleaved caspases-9, caspases-3 and PARP. Strikingly, overexpression of RAMP promoted anchorage-independent cell growth in soft agar.Conclusion: Our findings demonstrate that RAMP plays an oncogenic role in gastric carcinogenesis. Inhibition of RAMP may be a promising approach for gastric cancer therapy. © 2009 Cancer Research UK.
 
ISSN0007-0920
2013 Impact Factor: 4.817
 
DOIhttp://dx.doi.org/10.1038/sj.bjc.6605202
 
PubMed Central IDPMC2736823
 
ISI Accession Number IDWOS:000268861000019
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLi, J
 
dc.contributor.authorNg, EKO
 
dc.contributor.authorNg, YP
 
dc.contributor.authorWong, CYP
 
dc.contributor.authorYu, J
 
dc.contributor.authorJin, H
 
dc.contributor.authorCheng, VYY
 
dc.contributor.authorGo, MYY
 
dc.contributor.authorCheung, PKF
 
dc.contributor.authorEbert, MPA
 
dc.contributor.authorTong, J
 
dc.contributor.authorTo, KF
 
dc.contributor.authorChan, FKL
 
dc.contributor.authorSung, JJY
 
dc.contributor.authorIp, NY
 
dc.contributor.authorLeung, WK
 
dc.date.accessioned2010-09-17T10:43:17Z
 
dc.date.available2010-09-17T10:43:17Z
 
dc.date.issued2009
 
dc.description.abstractBackground: Retinoic acid-regulated nuclear matrix-associated protein (RAMP) is a WD40 repeat-containing protein that is involved in various biological functions, but little is known about its role in human cancer. This study aims to delineate the oncogenic role of RAMP in gastric carcinogenesis.Methods: RAMP expression was examined by real-time quantitative RT-PCR, immunohistochemistry and western blotting. Inhibition of RAMP expression was performed by siRNA-mediated knockdown. The functional effects of RAMP on cell kinetics were measured by cell viability assay, colony formation assay and flow cytometry. Cell lines stably expressing RAMP were established to investigate the oncogenic effects of RAMP in vitro.Results: Ramp was readily expressed in all seven gastric cancer cell lines and was significantly increased in human gastric cancer tissues when compared with their adjacent non-cancerous tissues (P0.001). In keeping with this, expression of RAMP protein was higher in gastric cancer tissues compared with their adjacent non-cancerous tissues, whereas moderate protein expression were noted in intestinal metaplasia. Knockdown of RAMP in gastric cancer cells significantly reduced cell proliferation (P0.01) and soft agar colony formation (P0.001), but induced apoptosis and G 2 /M arrest. In additional, knockdown RAMP induced cell apoptosis is dependent on functional accumulation of p53 and p21 and induction of cleaved caspases-9, caspases-3 and PARP. Strikingly, overexpression of RAMP promoted anchorage-independent cell growth in soft agar.Conclusion: Our findings demonstrate that RAMP plays an oncogenic role in gastric carcinogenesis. Inhibition of RAMP may be a promising approach for gastric cancer therapy. © 2009 Cancer Research UK.
 
dc.description.naturepublished_or_final_version
 
dc.identifier.citationBritish Journal Of Cancer, 2009, v. 101 n. 4, p. 691-698 [How to Cite?]
DOI: http://dx.doi.org/10.1038/sj.bjc.6605202
 
dc.identifier.doihttp://dx.doi.org/10.1038/sj.bjc.6605202
 
dc.identifier.epage698
 
dc.identifier.hkuros168713
 
dc.identifier.isiWOS:000268861000019
 
dc.identifier.issn0007-0920
2013 Impact Factor: 4.817
 
dc.identifier.issue4
 
dc.identifier.openurl
 
dc.identifier.pmcidPMC2736823
 
dc.identifier.pmid19672268
 
dc.identifier.scopuseid_2-s2.0-68749109533
 
dc.identifier.spage691
 
dc.identifier.urihttp://hdl.handle.net/10722/92344
 
dc.identifier.volume101
 
dc.languageeng
 
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjc
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofBritish Journal of Cancer
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshApoptosis - physiology
 
dc.subject.meshImmunohistochemistry
 
dc.subject.meshNuclear Proteins - genetics - metabolism
 
dc.subject.meshStomach Neoplasms - genetics - metabolism
 
dc.subject.meshTumor Markers, Biological - analysis
 
dc.subjectDTL/RAMP
 
dc.subjectL2DTL
 
dc.subjectOncogene
 
dc.subjectP21
 
dc.subjectP53
 
dc.subjectTumourigenesis
 
dc.titleIdentification of retinoic acid-regulated nuclear matrix-associated protein as a novel regulator of gastric cancer
 
dc.typeArticle
 
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Author Affiliations
  1. Prince of Wales Hospital Hong Kong
  2. Hong Kong University of Science and Technology
  3. Chinese University of Hong Kong
  4. Technische Universität München