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Article: Identification of retinoic acid-regulated nuclear matrix-associated protein as a novel regulator of gastric cancer

TitleIdentification of retinoic acid-regulated nuclear matrix-associated protein as a novel regulator of gastric cancer
Authors
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
Citation
British Journal Of Cancer, 2009, v. 101 n. 4, p. 691-698 How to Cite?
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.
Persistent Identifierhttp://hdl.handle.net/10722/92344
ISSN
2021 Impact Factor: 9.075
2020 SCImago Journal Rankings: 2.833
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, Jen_HK
dc.contributor.authorNg, EKOen_HK
dc.contributor.authorNg, YPen_HK
dc.contributor.authorWong, CYPen_HK
dc.contributor.authorYu, Jen_HK
dc.contributor.authorJin, Hen_HK
dc.contributor.authorCheng, VYYen_HK
dc.contributor.authorGo, MYYen_HK
dc.contributor.authorCheung, PKFen_HK
dc.contributor.authorEbert, MPAen_HK
dc.contributor.authorTong, Jen_HK
dc.contributor.authorTo, KFen_HK
dc.contributor.authorChan, FKLen_HK
dc.contributor.authorSung, JJYen_HK
dc.contributor.authorIp, NYen_HK
dc.contributor.authorLeung, WKen_HK
dc.date.accessioned2010-09-17T10:43:17Z-
dc.date.available2010-09-17T10:43:17Z-
dc.date.issued2009en_HK
dc.identifier.citationBritish Journal Of Cancer, 2009, v. 101 n. 4, p. 691-698en_HK
dc.identifier.issn0007-0920en_HK
dc.identifier.urihttp://hdl.handle.net/10722/92344-
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.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjcen_HK
dc.relation.ispartofBritish Journal of Canceren_HK
dc.subjectDTL/RAMPen_HK
dc.subjectL2DTLen_HK
dc.subjectOncogeneen_HK
dc.subjectP21en_HK
dc.subjectP53en_HK
dc.subjectTumourigenesisen_HK
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.titleIdentification of retinoic acid-regulated nuclear matrix-associated protein as a novel regulator of gastric canceren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0007-0920&volume=101&issue=4&spage=691&epage=698&date=2009&atitle=Identification+of+retinoic+acid-regulated+nuclear+matrix-associated+protein+as+a+novel+regulator+of+gastric+cancer-
dc.identifier.emailNg, EKO: ngko@hku.hken_HK
dc.identifier.emailLeung, WK: waikleung@hku.hken_HK
dc.identifier.authorityNg, EKO=rp01364en_HK
dc.identifier.authorityLeung, WK=rp01479en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1038/sj.bjc.6605202en_HK
dc.identifier.pmid19672268-
dc.identifier.pmcidPMC2736823-
dc.identifier.scopuseid_2-s2.0-68749109533en_HK
dc.identifier.hkuros168713-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-68749109533&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume101en_HK
dc.identifier.issue4en_HK
dc.identifier.spage691en_HK
dc.identifier.epage698en_HK
dc.identifier.isiWOS:000268861000019-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLi, J=36016939200en_HK
dc.identifier.scopusauthoridNg, EKO=21135553700en_HK
dc.identifier.scopusauthoridNg, YP=7202471018en_HK
dc.identifier.scopusauthoridWong, CYP=25947838400en_HK
dc.identifier.scopusauthoridYu, J=35351306800en_HK
dc.identifier.scopusauthoridJin, H=24577511700en_HK
dc.identifier.scopusauthoridCheng, VYY=8289922300en_HK
dc.identifier.scopusauthoridGo, MYY=7101882939en_HK
dc.identifier.scopusauthoridCheung, PKF=35108697100en_HK
dc.identifier.scopusauthoridEbert, MPA=35239660600en_HK
dc.identifier.scopusauthoridTong, J=7202724564en_HK
dc.identifier.scopusauthoridTo, KF=7101911940en_HK
dc.identifier.scopusauthoridChan, FKL=7202586434en_HK
dc.identifier.scopusauthoridSung, JJY=35405352400en_HK
dc.identifier.scopusauthoridIp, NY=7005756760en_HK
dc.identifier.scopusauthoridLeung, WK=7201504523en_HK
dc.identifier.issnl0007-0920-

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