Transduction effect of antisense K-ras on malignant phenotypes in gastric cancer cells
Identifieur interne : 003679 ( Main/Exploration ); précédent : 003678; suivant : 003680Transduction effect of antisense K-ras on malignant phenotypes in gastric cancer cells
Auteurs : Jae J. Song [Corée du Sud] ; Heuiran Lee [Corée du Sud] ; Eunhee Kim [Corée du Sud] ; Yeon S. Kim [Corée du Sud] ; Nae C. Yoo [Corée du Sud] ; Jae K. Roh [Corée du Sud] ; Byung S. Kim [Corée du Sud] ; Joohang Kim [Corée du Sud]Source :
- Cancer Letters [ 0304-3835 ] ; 2000.
English descriptors
- KwdEn :
- Teeft :
- Abdominal wall, Aberrant expression, Amersham pharmacia, Antisense, Antisense oligonucleotides, Antitumoral effects, Cancer cell lines, Cancer cells, Cancer letters, Cells transduced, Codon, Control group, Direct nucleotide sequencing, Direct sequencing analysis, Elsevier science ireland, Exon, Experimental group, Expression level, Expression levels, Gastric, Gastric cancer, Gastric cancer cell lines, Gastric cancer cells, Gastric cells, Genomic, Genomic dnas, Growth inhibition, Growth rate, Homozygous mutation, Human cancers, Human pancreatic cancer cell lines, Immunoblotting, Immunoblotting analysis, Initial mass, Korea research institute, Lncx, Lung cancer cells, Lysis buffer, Mutation, Neomycin phosphotransferase gene, Parental lane, Point mutation, Point mutations, Polymerase chain strand conformation polymorphism, Primer, Product sequencing, Recombinant retrovirus, Reduction rate, Retroviral vector, Retrovirus, Santa cruz, Sequencing, Sequencing primer, Several reports, Third exons, Transduced, Transduced cells, Tumor volume, Tumorigenicity, Wild type, Wild type gene, Yonsei cancer center, Yonsei university college.
Abstract
Abstract: The 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.
Url:
DOI: 10.1016/S0304-3835(00)00417-1
Affiliations:
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<term>Antisense oligonucleotides</term>
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<term>Gastric cancer</term>
<term>Gastric cancer cell lines</term>
<term>Gastric cancer cells</term>
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<term>Genomic dnas</term>
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<front><div type="abstract" xml:lang="en">Abstract: The 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.</div>
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