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1.
مقالة ي صينى | WPRIM | ID: wpr-1036205

الملخص

Objective @#To explore the association between mammalian sterile 20-like kinase 1(MST1)gene poly- morphism and haplotype and the risk of colorectal cancer,rectal cancer,and colon cancer in the Han population in Baotou area by case-control association study@*Methods @#A total of 390 patients with colorectal cancer diagnosed by pathology and 413 normal physical examination population were collected,and 2 ml of peripheral blood was taken for subsequent gene genotyping.Single nucleotide polymorphisms(SNPs)of MSTI gene were screened according to the genetic polymorphism data of Chinese Han population provided by the National Center for Biotechnology Information-Haplotype Mapping database.Gene genotyping was performed by Taqman method.Logistic regression was used to calculate the association between each SNP and the risk of colorectal cancer,colon cancer,and rectal cancer under codominant,dominant,overdominant,and recessive genetic models.@*Results @#Four SNPs of MSTI gene were screened,namely rs8000,rs2234197,rs2267853,and rs6073629.Among them,SNP rs2234197 was associated with the risk of rectal cancer.Compared with the GG+AA genotype,the AG genotype could reduce the risk of rectal cancer, OR[95%confidence interval(CI)]=0.657(0.442-0.976).SNP rs8000 was associated with the risk of colon cancer.Compared with the TT+GT genotype,theGG genotype could reduce the risk of colon cancer [OR(95%CI)=0.425(0.182, -0.992)].@*Conclusion @#MSTI gene SNP rs2234197 AG genotype and SNP rs8000 GG genotype may be protective factors for rectal cancer and colon cancer,respectively.

2.
مقالة ي صينى | WPRIM | ID: wpr-1038694

الملخص

Objective @#To investigate the association between single nucleotide polymorphism ( SNP) rs558614, rs9552315,rs7317471 and rs9509492 in large tumor suppressor kinase 2 (LATS2) gene and the risk of colorectal cancer.@*Methods @#A total of 390 colorectal cancer patients and 413 healthy subjects were genotyped by Taqman method.The odds ratio ( OR) and its 95% CI were calculated by unconditional logistic regression,to estimate the associations between SNP rs558614,rs9552315,rs7317471,rs9509492 in LATS2 gene and the risk of colorectal cancer,rectal cancer,as well as colon cancer under codominant,dominant,recessive,overdominant,and log-ad- ditive genetic models. Haplotypes were constructed by haploview software 4. 2 . @*Results @#SNP rs558614, rs7317471,rs9552315 and rs9509492 in LATS2 gene were not associated with the risk of colorectal cancer,rectal cancer and colon cancer under codominant,dominant,recessive,overdominant,and log-additive genetic models. No haploid blocks were formed between the 4 SNPs.@*Conclusion @#SNP rs558614 ,rs7317471 ,rs9552315, rs9509492 in LATS2 gene may not play a major role in the development of colorectal cancer,rectal cancer and co- lon cancer.

3.
Cancer Research and Treatment ; : 1162-1177, 2020.
مقالة ي 0 | WPRIM | ID: wpr-831142

الملخص

Purpose@#Fibroblast growth factor receptor 4 (FGFR4) plays a critical role in cancer progression involving in tumor proliferation, invasion, and metastasis. This study clarified the role of FGFR4-Arg388 variant in gastric cancer (GC), and more importantly highlighted the possibility of this single nucleotide polymorphism (SNP) as potential therapeutic targets. @*Materials and Methods@#FGFR4 polymorphism was characterized in advanced GC patients to perform statistical analysis. FGFR4-dependent signal pathways involving cell proliferation, invasion, migration, and resistance to oxaliplatin (OXA) in accordance with the SNP were also assessed in transfected GC cell lines. @*Results@#Among 102 GC patients, the FGFR4-Arg388 patients showed significantly higher tumor stage (p=0.047) and worse overall survival (p=0.033) than the Gly388 patients. Immunohistochemical results showed that FGFR4-Arg388 patients were more likely to have higher vimentin (p=0.025) and p-STAT3 (p=0.009) expression compared with FGFR4-Gly388 patients. In transfected GC cells, the overexpression of FGFR4-Arg388 variant increased proliferation and invasion of GC cells, increasing resistance of GC cells to OXA compared with cells overexpressing the Gly388 allele. @*Conclusion@#The exploration mechanism may be through FGFR4-Arg388/STAT3/epithelial to mesenchymal transition axis regulating pivotal oncogenic properties of GC cells. The FGFR4-Arg388 variant may be a biomarker and a candidate target for adjuvant treatment of GC.

4.
مقالة ي صينى | WPRIM | ID: wpr-594087

الملخص

BACKGROUND: Vascular endothelial growth factor (VEGF) is able to effectively treat the ischemic heart disease, but in vivo VEGF cannot be maintained effective concentration. OBJECTIVE: To detect the expression of VEGF mRNA and protein in human bone marrow mensenchymal stem cells transferred by VEGF-165 gene. DESIGN, TIME AND SETTING: The empirical study was conducted from March 2006 to April 2007 at Shanghai Chest Hospital. MATERIALS: Human bone marrow mesenchymal stem cell line and VEGF were offered by Basic Laboratory, Thoracic Tumor Institute, Shanghai Chest Hospital. METHODS: hVEGF165 gene was reconstructed in pcPGK-vector and transferred into human bone marrow mensenchymal stem cells (BMSCs) by liposome-mediated method, clone screening by G418. MAIN OUTCOME MEASURES: The mRNA and protein of VEGF gene in transferred cells was detected by reverse transcription-polymerase chain reaction (RT-PCR), Real time PCR, Western Blot, enzyme linked immunosorbent assay (ELISA) in 3 stem cells of pcPGK-VEGF165-IRES-GFP and pcPGK- IRES-GFP, respectively. RESULTS: pcPGK-hVEGF165 vector was reconstructed and transferred into hMSCs successfully. The expression of hVEGF165 in the transfected hMSCs was demonstrated with RT-PCR and Real time PCR. Western Blot and ELISA demonstrated that the expression of hVEGF165 in the transfected hMSCs and VEGF protein in supernatant were significantly more than untransfected hMSCs. CONCLUSION: hVEGF165 can be successfully transfected into BMSCs by using liposome mediated gene transfer. Stably expressed VEGF165 cell line can be obtained..

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