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DCXR promotes cell proliferation by promoting the activity of aerobic glycolysis in breast cancer

The function of human dicarbonyl/L-xylulose reductase (DCXR) in the pathophysiology of breast cancer is yet to be elucidated. The present study aimed to investigate the function of DCXR in glycolysis and the cell cycle of breast cancer cells with respect to cell proliferation. Differential expressed...

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Autores principales: Jin, Yongmei, Zhang, Miao, Tong, Yang, Qiu, Lin, Ye, Ying, Zhao, Bin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9827345/
https://www.ncbi.nlm.nih.gov/pubmed/36562355
http://dx.doi.org/10.3892/mmr.2022.12918
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author Jin, Yongmei
Zhang, Miao
Tong, Yang
Qiu, Lin
Ye, Ying
Zhao, Bin
author_facet Jin, Yongmei
Zhang, Miao
Tong, Yang
Qiu, Lin
Ye, Ying
Zhao, Bin
author_sort Jin, Yongmei
collection PubMed
description The function of human dicarbonyl/L-xylulose reductase (DCXR) in the pathophysiology of breast cancer is yet to be elucidated. The present study aimed to investigate the function of DCXR in glycolysis and the cell cycle of breast cancer cells with respect to cell proliferation. Differential expressed DCXR was identified in The Cancer Genome Atlas (TCGA) database and verified in clinical breast cancer tissue. DCXR silencing and overexpression were induced by RNA interference and lentiviral vectors, respectively. Cell cycle progression, proliferation and glycolytic activity of breast cancer cells were detected by flow cytometry, Cell Counting Kit-8 assay and chemical methods, respectively. Tumorigenicity was detected using nude mice xenograft models. The expression of DCXR was increased in TCGA breast cancer database and the function of DCXR was enriched in ‘glycolysis’ and ‘cell cycle’. Further analysis using clinical breast cancer samples confirmed upregulation of DCXR. The silencing of DCXR suppressed proliferation and cell cycle progression of breast cancer cells and significantly decreased the capacity for glycolysis, thereby demonstrating the effect of DCXR on the function of breast cancer cells. Similar conclusions were obtained in DCXR overexpressing cells; notably, DCXR overexpression promoted proliferation, cell cycle progression at S phase and glycolysis. 2-Deoxy-D-glucose inhibited the effect of DCXR on the proliferation and cell cycle progression of breast cancer cells. The present study revealed that DCXR regulated breast cancer cell cycle progression and proliferation by increasing glycolysis activity and thus may serve as an oncogene for breast cancer.
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spelling pubmed-98273452023-01-13 DCXR promotes cell proliferation by promoting the activity of aerobic glycolysis in breast cancer Jin, Yongmei Zhang, Miao Tong, Yang Qiu, Lin Ye, Ying Zhao, Bin Mol Med Rep Articles The function of human dicarbonyl/L-xylulose reductase (DCXR) in the pathophysiology of breast cancer is yet to be elucidated. The present study aimed to investigate the function of DCXR in glycolysis and the cell cycle of breast cancer cells with respect to cell proliferation. Differential expressed DCXR was identified in The Cancer Genome Atlas (TCGA) database and verified in clinical breast cancer tissue. DCXR silencing and overexpression were induced by RNA interference and lentiviral vectors, respectively. Cell cycle progression, proliferation and glycolytic activity of breast cancer cells were detected by flow cytometry, Cell Counting Kit-8 assay and chemical methods, respectively. Tumorigenicity was detected using nude mice xenograft models. The expression of DCXR was increased in TCGA breast cancer database and the function of DCXR was enriched in ‘glycolysis’ and ‘cell cycle’. Further analysis using clinical breast cancer samples confirmed upregulation of DCXR. The silencing of DCXR suppressed proliferation and cell cycle progression of breast cancer cells and significantly decreased the capacity for glycolysis, thereby demonstrating the effect of DCXR on the function of breast cancer cells. Similar conclusions were obtained in DCXR overexpressing cells; notably, DCXR overexpression promoted proliferation, cell cycle progression at S phase and glycolysis. 2-Deoxy-D-glucose inhibited the effect of DCXR on the proliferation and cell cycle progression of breast cancer cells. The present study revealed that DCXR regulated breast cancer cell cycle progression and proliferation by increasing glycolysis activity and thus may serve as an oncogene for breast cancer. D.A. Spandidos 2022-12-16 /pmc/articles/PMC9827345/ /pubmed/36562355 http://dx.doi.org/10.3892/mmr.2022.12918 Text en Copyright: © Jin et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , 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 Articles
Jin, Yongmei
Zhang, Miao
Tong, Yang
Qiu, Lin
Ye, Ying
Zhao, Bin
DCXR promotes cell proliferation by promoting the activity of aerobic glycolysis in breast cancer
title DCXR promotes cell proliferation by promoting the activity of aerobic glycolysis in breast cancer
title_full DCXR promotes cell proliferation by promoting the activity of aerobic glycolysis in breast cancer
title_fullStr DCXR promotes cell proliferation by promoting the activity of aerobic glycolysis in breast cancer
title_full_unstemmed DCXR promotes cell proliferation by promoting the activity of aerobic glycolysis in breast cancer
title_short DCXR promotes cell proliferation by promoting the activity of aerobic glycolysis in breast cancer
title_sort dcxr promotes cell proliferation by promoting the activity of aerobic glycolysis in breast cancer
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9827345/
https://www.ncbi.nlm.nih.gov/pubmed/36562355
http://dx.doi.org/10.3892/mmr.2022.12918
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