Transduction effect of antisense K-ras on malignant phenotypes in gastric cancer cells

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dc.contributor.authorJae J Song-
dc.contributor.authorHeui Ran Lee-
dc.contributor.authorEun Hee Kim-
dc.contributor.authorYeon Soo Kim-
dc.contributor.authorNae C Yoo-
dc.contributor.authorJae K Roh-
dc.contributor.authorByung S Kim-
dc.contributor.authorJoo Hang Kim-
dc.date.accessioned2017-04-19T08:56:51Z-
dc.date.available2017-04-19T08:56:51Z-
dc.date.issued2000-
dc.identifier.issn03043835-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/5004-
dc.description.abstractThe antitumoral effects of antisense RNA to K-ras were investigated in gastric cancer cell lines by examining the level of K-ras expression and the tumorigenicity in vitro and in vivo. Polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP), DNA sequencing, and immunoblotting analysis revealed that YCC-1 gastric cancer cells overexpressed wild type K-ras, whereas YCC-2 cells had a homozygous mutation in codon 12 from GGT (glycine) to AGT (serine), while SNU-1 cells had a heterozygous mutation to GAT (asparagine) in the identical position. Both YCC-1 and YCC-2 cells were transduced by LNC-AS/K-ras containing the antisense 2.2 kb genomic K-ras DNA fragment covering exon 2 and exon 3 specific for K-ras. The application of antisense K-ras significantly downregulated the expression of K-ras and had no influence on the expression of either H-ras or N-ras. The antisense-transduced YCC-2 cells grew considerably slower than the control group transduced by LNCX, whereas the growth inhibition of antisense-transduced YCC-1 cells was less prominent than that of transduced YCC-2 cells. In addition, the tumorigenicity of YCC-2 cells transduced by LNC-AS/K-ras was totally lost. Therefore, our results imply that the specific inhibition of K-ras p21 protein can be accomplished by introducing the antisense covering the K-ras- specific region to gastric cancer cells with aberrant K-ras expression, resulting in a reduction of the growth rate and suppression of tumorigenicity.-
dc.publisherElsevier-
dc.titleTransduction effect of antisense K-ras on malignant phenotypes in gastric cancer cells-
dc.title.alternativeTransduction effect of antisense K-ras on malignant phenotypes in gastric cancer cells-
dc.typeArticle-
dc.citation.titleCancer Letters-
dc.citation.number1-
dc.citation.endPage7-
dc.citation.startPage1-
dc.citation.volume157-
dc.contributor.alternativeName송재진-
dc.contributor.alternativeName이희란-
dc.contributor.alternativeName김은희-
dc.contributor.alternativeName김연수-
dc.contributor.alternativeName유내춘-
dc.contributor.alternativeName노재경-
dc.contributor.alternativeName김병수-
dc.contributor.alternativeName김주항-
dc.identifier.bibliographicCitationCancer Letters, vol. 157, no. 1, pp. 1-7-
dc.identifier.doi10.1016/S0304-3835(00)00417-1-
dc.subject.keywordgastric cancer-
dc.subject.keywordK-ras-
dc.subject.keywordantisense-
dc.subject.keywordgene therapy-
dc.subject.localgastric cancer-
dc.subject.localGastric cancer-
dc.subject.localK-ras-
dc.subject.localantisense-
dc.subject.localAntisense-
dc.subject.localgene therapy-
dc.subject.localGene therapy-
dc.description.journalClassY-
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