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miR-183-5p Promotes HCC Migration/Invasion via Increasing Aerobic Glycolysis
BACKGROUND: The mortality and morbidity of hepatocellular carcinoma (HCC) are still unacceptably high, despite decades of extensive studies. Aerobic glycolysis is a hallmark of cancer metabolism, closely relating to invasion and metastasis of HCC. MicroRNAs (miRNAs) are involved in the regulation of...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8187087/ https://www.ncbi.nlm.nih.gov/pubmed/34113130 http://dx.doi.org/10.2147/OTT.S304117 |
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author | Niu, Yaqian Liu, Fang Wang, Xiuyue Chang, Yuling Song, Yanmei Chu, Huiyuan Bao, Shisan Chen, Che |
author_facet | Niu, Yaqian Liu, Fang Wang, Xiuyue Chang, Yuling Song, Yanmei Chu, Huiyuan Bao, Shisan Chen, Che |
author_sort | Niu, Yaqian |
collection | PubMed |
description | BACKGROUND: The mortality and morbidity of hepatocellular carcinoma (HCC) are still unacceptably high, despite decades of extensive studies. Aerobic glycolysis is a hallmark of cancer metabolism, closely relating to invasion and metastasis of HCC. MicroRNAs (miRNAs) are involved in the regulation of aerobic glycolysis. miR-183-5p, an oncogenic miRNA, is highly expressed in HCC, but the regulatory mechanism of miR-183-5p in migration, invasion and aerobic glycolysis in HCC remains unclear. PURPOSE: To elucidate whether miR-183-5p affects aerobic glycolysis to regulate the migration and invasion of HCC, and to explore its regulatory mechanism. METHODS: We attempted to observe the effects of miR-183-5p on the migration and invasion of HepG2 cells by a wound-healing assay and Transwell assays. The effect of miR-183-5p on glycolysis was determined by glucose uptake and lactate generation. Western blot and qPCR were used to detect the relevant proteins and miRNA expression. RESULTS: Our results show that miR-183-5p promoted migration and invasion, enhanced glycolysis via increasing glucose uptake and lactate generation, and up-regulated glycolysis-related gene (PKM2, HK2, LDHA, GLUT1) expression in HepG2 cells. Further experiments indicated that miR-183-5p could decrease PTEN expression, but increased Akt, p-Akt and mTOR expression in HepG2 cells. CONCLUSION: These findings suggest that miR-183-5p may promote HCC migration and invasion via increasing aerobic glycolysis through targeting PTEN and then activating Akt/mTOR signaling. |
format | Online Article Text |
id | pubmed-8187087 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-81870872021-06-09 miR-183-5p Promotes HCC Migration/Invasion via Increasing Aerobic Glycolysis Niu, Yaqian Liu, Fang Wang, Xiuyue Chang, Yuling Song, Yanmei Chu, Huiyuan Bao, Shisan Chen, Che Onco Targets Ther Original Research BACKGROUND: The mortality and morbidity of hepatocellular carcinoma (HCC) are still unacceptably high, despite decades of extensive studies. Aerobic glycolysis is a hallmark of cancer metabolism, closely relating to invasion and metastasis of HCC. MicroRNAs (miRNAs) are involved in the regulation of aerobic glycolysis. miR-183-5p, an oncogenic miRNA, is highly expressed in HCC, but the regulatory mechanism of miR-183-5p in migration, invasion and aerobic glycolysis in HCC remains unclear. PURPOSE: To elucidate whether miR-183-5p affects aerobic glycolysis to regulate the migration and invasion of HCC, and to explore its regulatory mechanism. METHODS: We attempted to observe the effects of miR-183-5p on the migration and invasion of HepG2 cells by a wound-healing assay and Transwell assays. The effect of miR-183-5p on glycolysis was determined by glucose uptake and lactate generation. Western blot and qPCR were used to detect the relevant proteins and miRNA expression. RESULTS: Our results show that miR-183-5p promoted migration and invasion, enhanced glycolysis via increasing glucose uptake and lactate generation, and up-regulated glycolysis-related gene (PKM2, HK2, LDHA, GLUT1) expression in HepG2 cells. Further experiments indicated that miR-183-5p could decrease PTEN expression, but increased Akt, p-Akt and mTOR expression in HepG2 cells. CONCLUSION: These findings suggest that miR-183-5p may promote HCC migration and invasion via increasing aerobic glycolysis through targeting PTEN and then activating Akt/mTOR signaling. Dove 2021-06-04 /pmc/articles/PMC8187087/ /pubmed/34113130 http://dx.doi.org/10.2147/OTT.S304117 Text en © 2021 Niu et al. https://creativecommons.org/licenses/by-nc/3.0/This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/ (https://creativecommons.org/licenses/by-nc/3.0/) ). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Niu, Yaqian Liu, Fang Wang, Xiuyue Chang, Yuling Song, Yanmei Chu, Huiyuan Bao, Shisan Chen, Che miR-183-5p Promotes HCC Migration/Invasion via Increasing Aerobic Glycolysis |
title | miR-183-5p Promotes HCC Migration/Invasion via Increasing Aerobic Glycolysis |
title_full | miR-183-5p Promotes HCC Migration/Invasion via Increasing Aerobic Glycolysis |
title_fullStr | miR-183-5p Promotes HCC Migration/Invasion via Increasing Aerobic Glycolysis |
title_full_unstemmed | miR-183-5p Promotes HCC Migration/Invasion via Increasing Aerobic Glycolysis |
title_short | miR-183-5p Promotes HCC Migration/Invasion via Increasing Aerobic Glycolysis |
title_sort | mir-183-5p promotes hcc migration/invasion via increasing aerobic glycolysis |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8187087/ https://www.ncbi.nlm.nih.gov/pubmed/34113130 http://dx.doi.org/10.2147/OTT.S304117 |
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