author_facet Wang, Yajie
Wu, Shenshen
Yang, Xi
Li, Xiaobo
Chen, Rui
Wang, Yajie
Wu, Shenshen
Yang, Xi
Li, Xiaobo
Chen, Rui
author Wang, Yajie
Wu, Shenshen
Yang, Xi
Li, Xiaobo
Chen, Rui
spellingShingle Wang, Yajie
Wu, Shenshen
Yang, Xi
Li, Xiaobo
Chen, Rui
Bioscience Reports
Association between polymorphism in the promoter region of lncRNA GAS5 and the risk of colorectal cancer
Cell Biology
Molecular Biology
Biochemistry
Biophysics
author_sort wang, yajie
spelling Wang, Yajie Wu, Shenshen Yang, Xi Li, Xiaobo Chen, Rui 0144-8463 1573-4935 Portland Press Ltd. Cell Biology Molecular Biology Biochemistry Biophysics http://dx.doi.org/10.1042/bsr20190091 <jats:title>Abstract</jats:title> <jats:p>The growth arrest special 5 (GAS5), as a research hotspot of long noncoding RNAs (lncRNAs), has been reported to be associated with colorectal cancer (CRC). However, the association between polymorphisms in GAS5 and the risk of CRC was not clear. In the present study, a case–control study in 1078 CRC patients and 1175 matched healthy controls was performed to evaluate the association between the potential functional genetic variants in GAS5 and the risk of CRC. PCR-TaqMan, qPCR, dual-luciferase assay, electrophoretic mobility shift assay (EMSA), flow cytometry, migration and invasion assays were performed to evaluate the function of polymorphism. Results showed that subjects carrying the rs55829688 CT/TT genotypes had a significantly higher risk of CRC when compared with the CC genotype. Further qPCR assay confirmed that the CRC tissues with rs55829688 CT/TT genotypes had a higher GAS5 mRNA expression level. The dual-luciferase assay, qPCR and EMSA assay revealed that rs55829688 T&amp;gt;C polymorphism could decrease the expression level of GAS5 by impacting the binding ability of the transcription factor Yin Yang-1 (YY1) to the GAS5 promoter region. The expression of apoptosis-related proteins were detected by Western blot. Further, flow cytometry, migration, and invasion experiments showed that GAS5 repressed apoptosis and increased invasion and migration capability of CRC cells. Taken together, our findings provided evidence that the rs55829688 variant in the GAS5 promoter was associated with the risk of CRC and decreased expression of GAS5 by affecting the binding affinity of the transcription factors YY1 to GAS5.</jats:p> Association between polymorphism in the promoter region of lncRNA GAS5 and the risk of colorectal cancer Bioscience Reports
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title Association between polymorphism in the promoter region of lncRNA GAS5 and the risk of colorectal cancer
title_unstemmed Association between polymorphism in the promoter region of lncRNA GAS5 and the risk of colorectal cancer
title_full Association between polymorphism in the promoter region of lncRNA GAS5 and the risk of colorectal cancer
title_fullStr Association between polymorphism in the promoter region of lncRNA GAS5 and the risk of colorectal cancer
title_full_unstemmed Association between polymorphism in the promoter region of lncRNA GAS5 and the risk of colorectal cancer
title_short Association between polymorphism in the promoter region of lncRNA GAS5 and the risk of colorectal cancer
title_sort association between polymorphism in the promoter region of lncrna gas5 and the risk of colorectal cancer
topic Cell Biology
Molecular Biology
Biochemistry
Biophysics
url http://dx.doi.org/10.1042/bsr20190091
publishDate 2019
physical
description <jats:title>Abstract</jats:title> <jats:p>The growth arrest special 5 (GAS5), as a research hotspot of long noncoding RNAs (lncRNAs), has been reported to be associated with colorectal cancer (CRC). However, the association between polymorphisms in GAS5 and the risk of CRC was not clear. In the present study, a case–control study in 1078 CRC patients and 1175 matched healthy controls was performed to evaluate the association between the potential functional genetic variants in GAS5 and the risk of CRC. PCR-TaqMan, qPCR, dual-luciferase assay, electrophoretic mobility shift assay (EMSA), flow cytometry, migration and invasion assays were performed to evaluate the function of polymorphism. Results showed that subjects carrying the rs55829688 CT/TT genotypes had a significantly higher risk of CRC when compared with the CC genotype. Further qPCR assay confirmed that the CRC tissues with rs55829688 CT/TT genotypes had a higher GAS5 mRNA expression level. The dual-luciferase assay, qPCR and EMSA assay revealed that rs55829688 T&amp;gt;C polymorphism could decrease the expression level of GAS5 by impacting the binding ability of the transcription factor Yin Yang-1 (YY1) to the GAS5 promoter region. The expression of apoptosis-related proteins were detected by Western blot. Further, flow cytometry, migration, and invasion experiments showed that GAS5 repressed apoptosis and increased invasion and migration capability of CRC cells. Taken together, our findings provided evidence that the rs55829688 variant in the GAS5 promoter was associated with the risk of CRC and decreased expression of GAS5 by affecting the binding affinity of the transcription factors YY1 to GAS5.</jats:p>
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author Wang, Yajie, Wu, Shenshen, Yang, Xi, Li, Xiaobo, Chen, Rui
author_facet Wang, Yajie, Wu, Shenshen, Yang, Xi, Li, Xiaobo, Chen, Rui, Wang, Yajie, Wu, Shenshen, Yang, Xi, Li, Xiaobo, Chen, Rui
author_sort wang, yajie
container_issue 4
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container_title Bioscience Reports
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description <jats:title>Abstract</jats:title> <jats:p>The growth arrest special 5 (GAS5), as a research hotspot of long noncoding RNAs (lncRNAs), has been reported to be associated with colorectal cancer (CRC). However, the association between polymorphisms in GAS5 and the risk of CRC was not clear. In the present study, a case–control study in 1078 CRC patients and 1175 matched healthy controls was performed to evaluate the association between the potential functional genetic variants in GAS5 and the risk of CRC. PCR-TaqMan, qPCR, dual-luciferase assay, electrophoretic mobility shift assay (EMSA), flow cytometry, migration and invasion assays were performed to evaluate the function of polymorphism. Results showed that subjects carrying the rs55829688 CT/TT genotypes had a significantly higher risk of CRC when compared with the CC genotype. Further qPCR assay confirmed that the CRC tissues with rs55829688 CT/TT genotypes had a higher GAS5 mRNA expression level. The dual-luciferase assay, qPCR and EMSA assay revealed that rs55829688 T&amp;gt;C polymorphism could decrease the expression level of GAS5 by impacting the binding ability of the transcription factor Yin Yang-1 (YY1) to the GAS5 promoter region. The expression of apoptosis-related proteins were detected by Western blot. Further, flow cytometry, migration, and invasion experiments showed that GAS5 repressed apoptosis and increased invasion and migration capability of CRC cells. Taken together, our findings provided evidence that the rs55829688 variant in the GAS5 promoter was associated with the risk of CRC and decreased expression of GAS5 by affecting the binding affinity of the transcription factors YY1 to GAS5.</jats:p>
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spelling Wang, Yajie Wu, Shenshen Yang, Xi Li, Xiaobo Chen, Rui 0144-8463 1573-4935 Portland Press Ltd. Cell Biology Molecular Biology Biochemistry Biophysics http://dx.doi.org/10.1042/bsr20190091 <jats:title>Abstract</jats:title> <jats:p>The growth arrest special 5 (GAS5), as a research hotspot of long noncoding RNAs (lncRNAs), has been reported to be associated with colorectal cancer (CRC). However, the association between polymorphisms in GAS5 and the risk of CRC was not clear. In the present study, a case–control study in 1078 CRC patients and 1175 matched healthy controls was performed to evaluate the association between the potential functional genetic variants in GAS5 and the risk of CRC. PCR-TaqMan, qPCR, dual-luciferase assay, electrophoretic mobility shift assay (EMSA), flow cytometry, migration and invasion assays were performed to evaluate the function of polymorphism. Results showed that subjects carrying the rs55829688 CT/TT genotypes had a significantly higher risk of CRC when compared with the CC genotype. Further qPCR assay confirmed that the CRC tissues with rs55829688 CT/TT genotypes had a higher GAS5 mRNA expression level. The dual-luciferase assay, qPCR and EMSA assay revealed that rs55829688 T&amp;gt;C polymorphism could decrease the expression level of GAS5 by impacting the binding ability of the transcription factor Yin Yang-1 (YY1) to the GAS5 promoter region. The expression of apoptosis-related proteins were detected by Western blot. Further, flow cytometry, migration, and invasion experiments showed that GAS5 repressed apoptosis and increased invasion and migration capability of CRC cells. Taken together, our findings provided evidence that the rs55829688 variant in the GAS5 promoter was associated with the risk of CRC and decreased expression of GAS5 by affecting the binding affinity of the transcription factors YY1 to GAS5.</jats:p> Association between polymorphism in the promoter region of lncRNA GAS5 and the risk of colorectal cancer Bioscience Reports
spellingShingle Wang, Yajie, Wu, Shenshen, Yang, Xi, Li, Xiaobo, Chen, Rui, Bioscience Reports, Association between polymorphism in the promoter region of lncRNA GAS5 and the risk of colorectal cancer, Cell Biology, Molecular Biology, Biochemistry, Biophysics
title Association between polymorphism in the promoter region of lncRNA GAS5 and the risk of colorectal cancer
title_full Association between polymorphism in the promoter region of lncRNA GAS5 and the risk of colorectal cancer
title_fullStr Association between polymorphism in the promoter region of lncRNA GAS5 and the risk of colorectal cancer
title_full_unstemmed Association between polymorphism in the promoter region of lncRNA GAS5 and the risk of colorectal cancer
title_short Association between polymorphism in the promoter region of lncRNA GAS5 and the risk of colorectal cancer
title_sort association between polymorphism in the promoter region of lncrna gas5 and the risk of colorectal cancer
title_unstemmed Association between polymorphism in the promoter region of lncRNA GAS5 and the risk of colorectal cancer
topic Cell Biology, Molecular Biology, Biochemistry, Biophysics
url http://dx.doi.org/10.1042/bsr20190091