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The miR-383-LDHA axis regulates cell proliferation, invasion and glycolysis in hepatocellular cancer
OBJECTIVE(S): To explore the correlation between expression patterns and functions of miR-383 and LDHA in hepatocellular cancer (HCC). MATERIALS AND METHODS: We detected the expression of miR-383 and LDHA in 30 HCC tissues and their matched adjacent normal tissues using qRT-PCR. Then we performed MT...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Mashhad University of Medical Sciences
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5339660/ https://www.ncbi.nlm.nih.gov/pubmed/28293396 http://dx.doi.org/10.22038/ijbms.2017.8246 |
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author | Fang, Zhixiong He, Langqiu Jia, Hui Huang, Qiusheng Chen, Dan Zhang, Zhiwei |
author_facet | Fang, Zhixiong He, Langqiu Jia, Hui Huang, Qiusheng Chen, Dan Zhang, Zhiwei |
author_sort | Fang, Zhixiong |
collection | PubMed |
description | OBJECTIVE(S): To explore the correlation between expression patterns and functions of miR-383 and LDHA in hepatocellular cancer (HCC). MATERIALS AND METHODS: We detected the expression of miR-383 and LDHA in 30 HCC tissues and their matched adjacent normal tissues using qRT-PCR. Then we performed MTT assay, foci formation assay, transwell migration assay, glucose uptake assay and lactate production assay to explore the function of miR-383 in cell proliferation, invasion and glycolysis in HCC cell lines. Luciferase reporter assay was used to explore whether LDHA was a target gene of miR-383. Western blot and qRT-PCR were used to further confirm LDHA was targeted by miR-383. Then the above functional experiments were repeated to see whether the function of LDHA could be inhibited by miR-383. RESULTS: The results of qRT-PCR showed that miR-383 was down-regulated in HCC tissues compared with their matched adjacent normal tissues. Functional experiments showed that overexpression of miR-383 significantly suppressed cell proliferation, invasion and glycolysis. Luciferase reporter assay showed LDHA was a target gene of miR-383 and expression of LDHA was inversely correlated with that of miR-383 in HCC. Besides, increased cell proliferation, invasion and glycolysis triggered by LDHA could be inhibited by overexpression of miR-383 in HCC cell lines. CONCLUSION: Our study proved that miR-383 is down-regulated in HCC and acts as a tumor suppressor through targeting LDHA. Targeting the miR-383-LDHA axis might be a promising strategy in HCC treatment. |
format | Online Article Text |
id | pubmed-5339660 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Mashhad University of Medical Sciences |
record_format | MEDLINE/PubMed |
spelling | pubmed-53396602017-03-14 The miR-383-LDHA axis regulates cell proliferation, invasion and glycolysis in hepatocellular cancer Fang, Zhixiong He, Langqiu Jia, Hui Huang, Qiusheng Chen, Dan Zhang, Zhiwei Iran J Basic Med Sci Original Article OBJECTIVE(S): To explore the correlation between expression patterns and functions of miR-383 and LDHA in hepatocellular cancer (HCC). MATERIALS AND METHODS: We detected the expression of miR-383 and LDHA in 30 HCC tissues and their matched adjacent normal tissues using qRT-PCR. Then we performed MTT assay, foci formation assay, transwell migration assay, glucose uptake assay and lactate production assay to explore the function of miR-383 in cell proliferation, invasion and glycolysis in HCC cell lines. Luciferase reporter assay was used to explore whether LDHA was a target gene of miR-383. Western blot and qRT-PCR were used to further confirm LDHA was targeted by miR-383. Then the above functional experiments were repeated to see whether the function of LDHA could be inhibited by miR-383. RESULTS: The results of qRT-PCR showed that miR-383 was down-regulated in HCC tissues compared with their matched adjacent normal tissues. Functional experiments showed that overexpression of miR-383 significantly suppressed cell proliferation, invasion and glycolysis. Luciferase reporter assay showed LDHA was a target gene of miR-383 and expression of LDHA was inversely correlated with that of miR-383 in HCC. Besides, increased cell proliferation, invasion and glycolysis triggered by LDHA could be inhibited by overexpression of miR-383 in HCC cell lines. CONCLUSION: Our study proved that miR-383 is down-regulated in HCC and acts as a tumor suppressor through targeting LDHA. Targeting the miR-383-LDHA axis might be a promising strategy in HCC treatment. Mashhad University of Medical Sciences 2017-02 /pmc/articles/PMC5339660/ /pubmed/28293396 http://dx.doi.org/10.22038/ijbms.2017.8246 Text en Copyright: © Iranian Journal of Basic Medical Sciences http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Fang, Zhixiong He, Langqiu Jia, Hui Huang, Qiusheng Chen, Dan Zhang, Zhiwei The miR-383-LDHA axis regulates cell proliferation, invasion and glycolysis in hepatocellular cancer |
title | The miR-383-LDHA axis regulates cell proliferation, invasion and glycolysis in hepatocellular cancer |
title_full | The miR-383-LDHA axis regulates cell proliferation, invasion and glycolysis in hepatocellular cancer |
title_fullStr | The miR-383-LDHA axis regulates cell proliferation, invasion and glycolysis in hepatocellular cancer |
title_full_unstemmed | The miR-383-LDHA axis regulates cell proliferation, invasion and glycolysis in hepatocellular cancer |
title_short | The miR-383-LDHA axis regulates cell proliferation, invasion and glycolysis in hepatocellular cancer |
title_sort | mir-383-ldha axis regulates cell proliferation, invasion and glycolysis in hepatocellular cancer |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5339660/ https://www.ncbi.nlm.nih.gov/pubmed/28293396 http://dx.doi.org/10.22038/ijbms.2017.8246 |
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