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Autotaxin is a novel target of microRNA‐101‐3p

Autotaxin (ATX), a vital enzyme that generates lysophosphatidic acid (LPA), affects many biological processes, including tumorigenesis, via the ATX–LPA axis. In this study, we demonstrate that microRNA‐101‐3p (miR‐101‐3p), a well‐known tumor suppressor, downregulates ATX expression at the posttransc...

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Detalles Bibliográficos
Autores principales: Wang, Yuqin, Lyu, Lin, Zhang, Xiaotian, Zhang, Junjie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6443858/
https://www.ncbi.nlm.nih.gov/pubmed/30984544
http://dx.doi.org/10.1002/2211-5463.12608
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author Wang, Yuqin
Lyu, Lin
Zhang, Xiaotian
Zhang, Junjie
author_facet Wang, Yuqin
Lyu, Lin
Zhang, Xiaotian
Zhang, Junjie
author_sort Wang, Yuqin
collection PubMed
description Autotaxin (ATX), a vital enzyme that generates lysophosphatidic acid (LPA), affects many biological processes, including tumorigenesis, via the ATX–LPA axis. In this study, we demonstrate that microRNA‐101‐3p (miR‐101‐3p), a well‐known tumor suppressor, downregulates ATX expression at the posttranscriptional level. We found that miR‐101‐3p inhibits ATX regulation by directly targeting a conserved sequence in the ATX mRNA 3′UTR. Moreover, we observed an inverse correlation between ATX and miR‐101‐3p levels in various types of cancer cells. ATX is highly expressed in several human cancers. Here, we verified that ATX expression is significantly inhibited by miR‐101‐3p in U87 and HCT116 cells. ATX downregulation contributed to the suppression of migration, invasion, and proliferation mediated by miR‐101‐3p; furthermore, the tumor‐suppressing activity of miR‐101‐3p was partially reduced by the addition of LPA in U87 cells. Our data suggest that ATX is a novel target of miR‐101‐3p.
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spelling pubmed-64438582019-04-12 Autotaxin is a novel target of microRNA‐101‐3p Wang, Yuqin Lyu, Lin Zhang, Xiaotian Zhang, Junjie FEBS Open Bio Research Articles Autotaxin (ATX), a vital enzyme that generates lysophosphatidic acid (LPA), affects many biological processes, including tumorigenesis, via the ATX–LPA axis. In this study, we demonstrate that microRNA‐101‐3p (miR‐101‐3p), a well‐known tumor suppressor, downregulates ATX expression at the posttranscriptional level. We found that miR‐101‐3p inhibits ATX regulation by directly targeting a conserved sequence in the ATX mRNA 3′UTR. Moreover, we observed an inverse correlation between ATX and miR‐101‐3p levels in various types of cancer cells. ATX is highly expressed in several human cancers. Here, we verified that ATX expression is significantly inhibited by miR‐101‐3p in U87 and HCT116 cells. ATX downregulation contributed to the suppression of migration, invasion, and proliferation mediated by miR‐101‐3p; furthermore, the tumor‐suppressing activity of miR‐101‐3p was partially reduced by the addition of LPA in U87 cells. Our data suggest that ATX is a novel target of miR‐101‐3p. John Wiley and Sons Inc. 2019-03-01 /pmc/articles/PMC6443858/ /pubmed/30984544 http://dx.doi.org/10.1002/2211-5463.12608 Text en © 2019 The Authors. Published by FEBS Press and John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Articles
Wang, Yuqin
Lyu, Lin
Zhang, Xiaotian
Zhang, Junjie
Autotaxin is a novel target of microRNA‐101‐3p
title Autotaxin is a novel target of microRNA‐101‐3p
title_full Autotaxin is a novel target of microRNA‐101‐3p
title_fullStr Autotaxin is a novel target of microRNA‐101‐3p
title_full_unstemmed Autotaxin is a novel target of microRNA‐101‐3p
title_short Autotaxin is a novel target of microRNA‐101‐3p
title_sort autotaxin is a novel target of microrna‐101‐3p
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6443858/
https://www.ncbi.nlm.nih.gov/pubmed/30984544
http://dx.doi.org/10.1002/2211-5463.12608
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