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C-myc/TSPEAR-AS2 Axis Facilitates Breast Cancer Growth and Metastasis in a GLUT1-Dependent Glycolysis Manner
A large number of facts have shown that epigenetic modification and metabolic reprogramming represented by noncoding RNA play an important role in the invasion and metastasis of breast cancer, but the mechanism is not clear. The purpose of our study is to find a new biomarker of breast cancer and to...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9187470/ https://www.ncbi.nlm.nih.gov/pubmed/35692593 http://dx.doi.org/10.1155/2022/4239500 |
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author | Xu, Jian Li, Tao Zhang, Yang Qiu, Donghai Chen, Nan Chai, Xupeng PengLi, Li, Jia |
author_facet | Xu, Jian Li, Tao Zhang, Yang Qiu, Donghai Chen, Nan Chai, Xupeng PengLi, Li, Jia |
author_sort | Xu, Jian |
collection | PubMed |
description | A large number of facts have shown that epigenetic modification and metabolic reprogramming represented by noncoding RNA play an important role in the invasion and metastasis of breast cancer, but the mechanism is not clear. The purpose of our study is to find a new biomarker of breast cancer and to provide a new perspective for regulating glucose metabolism and aerobic glycolysis of BC. In this paper, by downregulating C-myc protein, our team found that the expression of long-chain noncoding RNATSPAR-AS2 was significantly downregulated. However, the expression of long-chain noncoding RNASPAR-AS2 in BC is relatively high, and the prognosis is poor. TSPEAR-AS2 can promote the malignant phenotype of BC cells, including proliferation, apoptosis, invasion and metastasis, and glycolysis. At the same time, TSPEAR-AS2 can also upregulate the expression of GLUT1, an important regulator of glycolysis, thus promoting the metabolic reprogramming of BC. Molecular mechanism experiments show that TSPEAR-AS2 may promote the expression of GLUT1 by participating in IGF2BP2 modified by the GLUT1 gene. Our results suggest that the C-myc/TSPEAR-AS2/GLUT1 axis promotes the invasion and metastasis of BC by inducing glucose metabolism reprogramming. However, more phenotypic and molecular mechanism results need to be further verified. |
format | Online Article Text |
id | pubmed-9187470 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-91874702022-06-11 C-myc/TSPEAR-AS2 Axis Facilitates Breast Cancer Growth and Metastasis in a GLUT1-Dependent Glycolysis Manner Xu, Jian Li, Tao Zhang, Yang Qiu, Donghai Chen, Nan Chai, Xupeng PengLi, Li, Jia Biomed Res Int Research Article A large number of facts have shown that epigenetic modification and metabolic reprogramming represented by noncoding RNA play an important role in the invasion and metastasis of breast cancer, but the mechanism is not clear. The purpose of our study is to find a new biomarker of breast cancer and to provide a new perspective for regulating glucose metabolism and aerobic glycolysis of BC. In this paper, by downregulating C-myc protein, our team found that the expression of long-chain noncoding RNATSPAR-AS2 was significantly downregulated. However, the expression of long-chain noncoding RNASPAR-AS2 in BC is relatively high, and the prognosis is poor. TSPEAR-AS2 can promote the malignant phenotype of BC cells, including proliferation, apoptosis, invasion and metastasis, and glycolysis. At the same time, TSPEAR-AS2 can also upregulate the expression of GLUT1, an important regulator of glycolysis, thus promoting the metabolic reprogramming of BC. Molecular mechanism experiments show that TSPEAR-AS2 may promote the expression of GLUT1 by participating in IGF2BP2 modified by the GLUT1 gene. Our results suggest that the C-myc/TSPEAR-AS2/GLUT1 axis promotes the invasion and metastasis of BC by inducing glucose metabolism reprogramming. However, more phenotypic and molecular mechanism results need to be further verified. Hindawi 2022-06-03 /pmc/articles/PMC9187470/ /pubmed/35692593 http://dx.doi.org/10.1155/2022/4239500 Text en Copyright © 2022 Jian Xu et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Xu, Jian Li, Tao Zhang, Yang Qiu, Donghai Chen, Nan Chai, Xupeng PengLi, Li, Jia C-myc/TSPEAR-AS2 Axis Facilitates Breast Cancer Growth and Metastasis in a GLUT1-Dependent Glycolysis Manner |
title | C-myc/TSPEAR-AS2 Axis Facilitates Breast Cancer Growth and Metastasis in a GLUT1-Dependent Glycolysis Manner |
title_full | C-myc/TSPEAR-AS2 Axis Facilitates Breast Cancer Growth and Metastasis in a GLUT1-Dependent Glycolysis Manner |
title_fullStr | C-myc/TSPEAR-AS2 Axis Facilitates Breast Cancer Growth and Metastasis in a GLUT1-Dependent Glycolysis Manner |
title_full_unstemmed | C-myc/TSPEAR-AS2 Axis Facilitates Breast Cancer Growth and Metastasis in a GLUT1-Dependent Glycolysis Manner |
title_short | C-myc/TSPEAR-AS2 Axis Facilitates Breast Cancer Growth and Metastasis in a GLUT1-Dependent Glycolysis Manner |
title_sort | c-myc/tspear-as2 axis facilitates breast cancer growth and metastasis in a glut1-dependent glycolysis manner |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9187470/ https://www.ncbi.nlm.nih.gov/pubmed/35692593 http://dx.doi.org/10.1155/2022/4239500 |
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