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Article: Identification and characterization of a novel melanoma tumor suppressor gene on human chromosome 6q21

TitleIdentification and characterization of a novel melanoma tumor suppressor gene on human chromosome 6q21
Authors
Issue Date2009
PublisherAmerican Association for Cancer Research
Citation
Clinical Cancer Research, 2009, v. 15 n. 3, p. 797-803 How to Cite?
AbstractPurpose: By characterizing a complex chromosome rearrangement involving 6q and 17p in melanoma cell line UACC-930, we isolated a candidate tumor suppressor gene at 6q21, named prenyl diphosphate synthase subunit 2 (PDSS2), which was interrupted by an inversion breakpoint. The purpose of this study was to determine the tumor-suppressive potential of PDSS2 in the development of melanoma. Experimental Design: To isolate the rearranged 6q in UACC-930 cells, a bacterial artificial chromosome clone (RP1-67A8) covering the breakpoint at 6q21 was digested with Hind Ill and each DNA fragment was used as the probe for the breakpoint in Southern blotting. The Hind Ill fragment probe covering the breakpoint was then used to screen an Eco Rl-digested DNA library generated from UACC-930. To characterize the tumor-suppressive potential of PDSS2, PDSS2 was stably transfected into a highly tumorigenic melanoma cell line, UACC-903. The tumor-suppressive function of PDSS2 was shown by both in vitro and in vivo assays. The differential expression of PDSS2 in benign nevi and primary melanoma samples was also studied. Results: Down-regulation of PDSS2 was observed in 59 of 87 (67.8%) primary melanomas, which was significantly higher than that in benign nevi (7 of 66,10.6%; P < 0.001). ln addition, an overexpression of the PDSS2 in UACC-903 cells could inhibit tumor cell growth, decrease the colony-forming ability in soft agar, and totally abrogate the tumorigenicity of UACC-903 in nude mice. Conclusions: Our results support the proposal that PDSS2 is a novel tumor suppressor gene that plays an important role in the development of malignant melanoma. © 2009 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/60441
ISSN
2015 Impact Factor: 8.738
2015 SCImago Journal Rankings: 5.314
ISI Accession Number ID
Funding AgencyGrant Number
Leung Kwok Tze Foundation
Sun Yat-sen University "Hundred Talents Program"85000 3171311
Major State Basic Research Program of China2006CB910104
Funding Information:

Leung Kwok Tze Foundation, Sun Yat-sen University "Hundred Talents Program" (85000 3171311), and The Major State Basic Research Program of China (2006CB910104).

References

 

DC FieldValueLanguage
dc.contributor.authorFung, JMWen_HK
dc.contributor.authorSmith, Ren_HK
dc.contributor.authorBrown, MAen_HK
dc.contributor.authorLau, SHen_HK
dc.contributor.authorXie, Den_HK
dc.contributor.authorLau, GKen_HK
dc.contributor.authorGuan, XYen_HK
dc.date.accessioned2010-05-31T04:10:51Z-
dc.date.available2010-05-31T04:10:51Z-
dc.date.issued2009en_HK
dc.identifier.citationClinical Cancer Research, 2009, v. 15 n. 3, p. 797-803en_HK
dc.identifier.issn1078-0432en_HK
dc.identifier.urihttp://hdl.handle.net/10722/60441-
dc.description.abstractPurpose: By characterizing a complex chromosome rearrangement involving 6q and 17p in melanoma cell line UACC-930, we isolated a candidate tumor suppressor gene at 6q21, named prenyl diphosphate synthase subunit 2 (PDSS2), which was interrupted by an inversion breakpoint. The purpose of this study was to determine the tumor-suppressive potential of PDSS2 in the development of melanoma. Experimental Design: To isolate the rearranged 6q in UACC-930 cells, a bacterial artificial chromosome clone (RP1-67A8) covering the breakpoint at 6q21 was digested with Hind Ill and each DNA fragment was used as the probe for the breakpoint in Southern blotting. The Hind Ill fragment probe covering the breakpoint was then used to screen an Eco Rl-digested DNA library generated from UACC-930. To characterize the tumor-suppressive potential of PDSS2, PDSS2 was stably transfected into a highly tumorigenic melanoma cell line, UACC-903. The tumor-suppressive function of PDSS2 was shown by both in vitro and in vivo assays. The differential expression of PDSS2 in benign nevi and primary melanoma samples was also studied. Results: Down-regulation of PDSS2 was observed in 59 of 87 (67.8%) primary melanomas, which was significantly higher than that in benign nevi (7 of 66,10.6%; P < 0.001). ln addition, an overexpression of the PDSS2 in UACC-903 cells could inhibit tumor cell growth, decrease the colony-forming ability in soft agar, and totally abrogate the tumorigenicity of UACC-903 in nude mice. Conclusions: Our results support the proposal that PDSS2 is a novel tumor suppressor gene that plays an important role in the development of malignant melanoma. © 2009 American Association for Cancer Research.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Researchen_HK
dc.relation.ispartofClinical Cancer Researchen_HK
dc.subject.meshAlkyl and Aryl Transferases - geneticsen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBase Sequenceen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshChromosome Breakageen_HK
dc.subject.meshChromosomes, Human, Pair 6en_HK
dc.subject.meshDown-Regulationen_HK
dc.subject.meshGenes, Tumor Suppressoren_HK
dc.subject.meshHumansen_HK
dc.subject.meshMelanoma - geneticsen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Nudeen_HK
dc.subject.meshMolecular Sequence Dataen_HK
dc.subject.meshNeoplasm Transplantationen_HK
dc.subject.meshSkin Neoplasms - geneticsen_HK
dc.titleIdentification and characterization of a novel melanoma tumor suppressor gene on human chromosome 6q21en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1078-0432&volume=15&spage=797&epage=803&date=2009&atitle=Identification+and+characterization+of+a+novel+melanoma+tumor+suppressor+gene+on+human+chromosome+6q21en_HK
dc.identifier.emailGuan, XY:xyguan@hkucc.hku.hken_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1158/1078-0432.CCR-08-1472en_HK
dc.identifier.pmid19188149-
dc.identifier.scopuseid_2-s2.0-61349098014en_HK
dc.identifier.hkuros156535en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-61349098014&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume15en_HK
dc.identifier.issue3en_HK
dc.identifier.spage797en_HK
dc.identifier.epage803en_HK
dc.identifier.isiWOS:000263213600008-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridFung, JMW=23469161200en_HK
dc.identifier.scopusauthoridSmith, R=7410292253en_HK
dc.identifier.scopusauthoridBrown, MA=34567480000en_HK
dc.identifier.scopusauthoridLau, SH=7401596190en_HK
dc.identifier.scopusauthoridXie, D=35070710200en_HK
dc.identifier.scopusauthoridLau, GK=7102301257en_HK
dc.identifier.scopusauthoridGuan, XY=7201463221en_HK

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