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OGG1 contributes to hepatocellular carcinoma by promoting cell cycle‐related protein expression and enhancing DNA oxidative damage repair in tumor cells
BACKGROUND: This study aimed to analyze the expression of 8‐oxoguanine DNA glycosylase (OGG1) in patients with hepatocellular carcinoma (HCC) and its effect on prognosis by bioinformatics techniques and to determine its possible carcinogenic mechanism through data mining. METHODS: The difference in...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9279955/ https://www.ncbi.nlm.nih.gov/pubmed/35723423 http://dx.doi.org/10.1002/jcla.24561 |
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author | Zhang, He Jiang, Peng‐jun Lv, Meng‐yuan Zhao, Yan‐hua Cui, Ju Chen, Jie |
author_facet | Zhang, He Jiang, Peng‐jun Lv, Meng‐yuan Zhao, Yan‐hua Cui, Ju Chen, Jie |
author_sort | Zhang, He |
collection | PubMed |
description | BACKGROUND: This study aimed to analyze the expression of 8‐oxoguanine DNA glycosylase (OGG1) in patients with hepatocellular carcinoma (HCC) and its effect on prognosis by bioinformatics techniques and to determine its possible carcinogenic mechanism through data mining. METHODS: The difference in OGG1 expression between healthy people and HCC patients was searched and analyzed by TCGA and GEO databases, and the effect of OGG1 on prognosis was judged by survival analysis. Meanwhile, the possible molecular mechanism of OGG1 in the tumorigenesis and development of HCC was explored by GO analysis, KEGG analysis, immune infiltration analysis, protein–protein interaction network, promoter methylation analysis, and so forth. Quantitative polymerase chain reaction (qPCR) was used to examine the gene expression in 36 pairs of HCC tissues and adjacent tissues. RESULTS: The expression of OGG1 in HCC patients was higher than that in healthy people, and the overexpression of OGG1 might stimulate cell proliferation by increasing the activity of cell cycle‐related proteins. CONCLUSION: The alteration of OGG1 was significantly correlated with the tumorigenesis and development of HCC. OGG1 is expected to be a new biomarker for evaluating the prognosis of HCC and a new target for the treatment of HCC. |
format | Online Article Text |
id | pubmed-9279955 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-92799552022-07-15 OGG1 contributes to hepatocellular carcinoma by promoting cell cycle‐related protein expression and enhancing DNA oxidative damage repair in tumor cells Zhang, He Jiang, Peng‐jun Lv, Meng‐yuan Zhao, Yan‐hua Cui, Ju Chen, Jie J Clin Lab Anal Research Articles BACKGROUND: This study aimed to analyze the expression of 8‐oxoguanine DNA glycosylase (OGG1) in patients with hepatocellular carcinoma (HCC) and its effect on prognosis by bioinformatics techniques and to determine its possible carcinogenic mechanism through data mining. METHODS: The difference in OGG1 expression between healthy people and HCC patients was searched and analyzed by TCGA and GEO databases, and the effect of OGG1 on prognosis was judged by survival analysis. Meanwhile, the possible molecular mechanism of OGG1 in the tumorigenesis and development of HCC was explored by GO analysis, KEGG analysis, immune infiltration analysis, protein–protein interaction network, promoter methylation analysis, and so forth. Quantitative polymerase chain reaction (qPCR) was used to examine the gene expression in 36 pairs of HCC tissues and adjacent tissues. RESULTS: The expression of OGG1 in HCC patients was higher than that in healthy people, and the overexpression of OGG1 might stimulate cell proliferation by increasing the activity of cell cycle‐related proteins. CONCLUSION: The alteration of OGG1 was significantly correlated with the tumorigenesis and development of HCC. OGG1 is expected to be a new biomarker for evaluating the prognosis of HCC and a new target for the treatment of HCC. John Wiley and Sons Inc. 2022-06-19 /pmc/articles/PMC9279955/ /pubmed/35723423 http://dx.doi.org/10.1002/jcla.24561 Text en © 2022 The Authors. Journal of Clinical Laboratory Analysis published by Wiley Periodicals LLC. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. |
spellingShingle | Research Articles Zhang, He Jiang, Peng‐jun Lv, Meng‐yuan Zhao, Yan‐hua Cui, Ju Chen, Jie OGG1 contributes to hepatocellular carcinoma by promoting cell cycle‐related protein expression and enhancing DNA oxidative damage repair in tumor cells |
title |
OGG1 contributes to hepatocellular carcinoma by promoting cell cycle‐related protein expression and enhancing DNA oxidative damage repair in tumor cells |
title_full |
OGG1 contributes to hepatocellular carcinoma by promoting cell cycle‐related protein expression and enhancing DNA oxidative damage repair in tumor cells |
title_fullStr |
OGG1 contributes to hepatocellular carcinoma by promoting cell cycle‐related protein expression and enhancing DNA oxidative damage repair in tumor cells |
title_full_unstemmed |
OGG1 contributes to hepatocellular carcinoma by promoting cell cycle‐related protein expression and enhancing DNA oxidative damage repair in tumor cells |
title_short |
OGG1 contributes to hepatocellular carcinoma by promoting cell cycle‐related protein expression and enhancing DNA oxidative damage repair in tumor cells |
title_sort | ogg1 contributes to hepatocellular carcinoma by promoting cell cycle‐related protein expression and enhancing dna oxidative damage repair in tumor cells |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9279955/ https://www.ncbi.nlm.nih.gov/pubmed/35723423 http://dx.doi.org/10.1002/jcla.24561 |
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