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Circ_0058063 upregulates GLUT1 expression and promotes glucose-uptake in esophageal squamous-cell carcinomas
BACKGROUND: CirRNA Circ_0058063 has been proven as an oncogene in bladder cancer, while its involvement in esophageal squamous-cell carcinomas (ESCC) is unknown. This study aimed to investigate the role of Circ_0058063 in ESCC. METHODS: Paired ESCC and non-tumor tissues were collected from ESCC pati...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
AME Publishing Company
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7139087/ https://www.ncbi.nlm.nih.gov/pubmed/32274160 http://dx.doi.org/10.21037/jtd.2019.12.57 |
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author | Zheng, Yinbin Chen, Yi Jiang, Hongjing Zhang, Hongdian Wang, Hua Xu, Jun Yu, Zhentao |
author_facet | Zheng, Yinbin Chen, Yi Jiang, Hongjing Zhang, Hongdian Wang, Hua Xu, Jun Yu, Zhentao |
author_sort | Zheng, Yinbin |
collection | PubMed |
description | BACKGROUND: CirRNA Circ_0058063 has been proven as an oncogene in bladder cancer, while its involvement in esophageal squamous-cell carcinomas (ESCC) is unknown. This study aimed to investigate the role of Circ_0058063 in ESCC. METHODS: Paired ESCC and non-tumor tissues were collected from ESCC patients and gene expression was analyzed by quantitative reverse transcription polymerase chain reaction (RT-qPCR). Gene interactions were analyzed by overexpression experiment. Glucose uptake was analyzed by glucose uptake assay. Cell proliferation was analyzed by cell proliferation assay. RESULTS: We found that Circ_0058063 was upregulated in ESCC and positively correlated with GLUT1 mRNA. It is known that GLUT1 plays critical roles in glucose transportation and glucose supports the Warburg Effect as the major metabolic precursor. In ESCC cells, Circ_0058063 and GLUT1 overexpression both promoted glucose uptake. In ECSS cells, Circ_0058063 overexpression resulted in the upregulated, while Circ_0058063 knockdown resulted in downregulated GLUT1. In cell proliferation assay, Circ_0058063 and GLUT1 overexpression resulted in the increased, while Circ_0058063 knockdown resulted in the decreased rate of ESCC cell proliferation. Moreover, GLUT1 overexpression reduced the effects of Circ_0058063 knockdown. CONCLUSIONS: Circ_0058063 upregulates GLUT1 expression and promotes glucose-uptake in ESCC to promote cell proliferation. |
format | Online Article Text |
id | pubmed-7139087 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | AME Publishing Company |
record_format | MEDLINE/PubMed |
spelling | pubmed-71390872020-04-09 Circ_0058063 upregulates GLUT1 expression and promotes glucose-uptake in esophageal squamous-cell carcinomas Zheng, Yinbin Chen, Yi Jiang, Hongjing Zhang, Hongdian Wang, Hua Xu, Jun Yu, Zhentao J Thorac Dis Original Article BACKGROUND: CirRNA Circ_0058063 has been proven as an oncogene in bladder cancer, while its involvement in esophageal squamous-cell carcinomas (ESCC) is unknown. This study aimed to investigate the role of Circ_0058063 in ESCC. METHODS: Paired ESCC and non-tumor tissues were collected from ESCC patients and gene expression was analyzed by quantitative reverse transcription polymerase chain reaction (RT-qPCR). Gene interactions were analyzed by overexpression experiment. Glucose uptake was analyzed by glucose uptake assay. Cell proliferation was analyzed by cell proliferation assay. RESULTS: We found that Circ_0058063 was upregulated in ESCC and positively correlated with GLUT1 mRNA. It is known that GLUT1 plays critical roles in glucose transportation and glucose supports the Warburg Effect as the major metabolic precursor. In ESCC cells, Circ_0058063 and GLUT1 overexpression both promoted glucose uptake. In ECSS cells, Circ_0058063 overexpression resulted in the upregulated, while Circ_0058063 knockdown resulted in downregulated GLUT1. In cell proliferation assay, Circ_0058063 and GLUT1 overexpression resulted in the increased, while Circ_0058063 knockdown resulted in the decreased rate of ESCC cell proliferation. Moreover, GLUT1 overexpression reduced the effects of Circ_0058063 knockdown. CONCLUSIONS: Circ_0058063 upregulates GLUT1 expression and promotes glucose-uptake in ESCC to promote cell proliferation. AME Publishing Company 2020-03 /pmc/articles/PMC7139087/ /pubmed/32274160 http://dx.doi.org/10.21037/jtd.2019.12.57 Text en 2020 Journal of Thoracic Disease. All rights reserved. https://creativecommons.org/licenses/by-nc-nd/4.0/Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) . |
spellingShingle | Original Article Zheng, Yinbin Chen, Yi Jiang, Hongjing Zhang, Hongdian Wang, Hua Xu, Jun Yu, Zhentao Circ_0058063 upregulates GLUT1 expression and promotes glucose-uptake in esophageal squamous-cell carcinomas |
title | Circ_0058063 upregulates GLUT1 expression and promotes glucose-uptake in esophageal squamous-cell carcinomas |
title_full | Circ_0058063 upregulates GLUT1 expression and promotes glucose-uptake in esophageal squamous-cell carcinomas |
title_fullStr | Circ_0058063 upregulates GLUT1 expression and promotes glucose-uptake in esophageal squamous-cell carcinomas |
title_full_unstemmed | Circ_0058063 upregulates GLUT1 expression and promotes glucose-uptake in esophageal squamous-cell carcinomas |
title_short | Circ_0058063 upregulates GLUT1 expression and promotes glucose-uptake in esophageal squamous-cell carcinomas |
title_sort | circ_0058063 upregulates glut1 expression and promotes glucose-uptake in esophageal squamous-cell carcinomas |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7139087/ https://www.ncbi.nlm.nih.gov/pubmed/32274160 http://dx.doi.org/10.21037/jtd.2019.12.57 |
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