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MiR-320 inhibits the growth of glioma cells through downregulating PBX3

BACKGROUND: MiR-320 is downregulated in multiple cancers, including glioma and acts as tumor suppressor through inhibiting tumor cells proliferation and inducing apoptosis. PBX3 (Pre-B cell leukemia homeobox 3), a putative target gene of miR-320, has been reported to be upregulated in various tumors...

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Autores principales: Pan, Cuicui, Gao, Hua, Zheng, Ni, Gao, Qi, Si, Yuanquan, Zhao, Yueran
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5609034/
https://www.ncbi.nlm.nih.gov/pubmed/28934982
http://dx.doi.org/10.1186/s40659-017-0137-4
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author Pan, Cuicui
Gao, Hua
Zheng, Ni
Gao, Qi
Si, Yuanquan
Zhao, Yueran
author_facet Pan, Cuicui
Gao, Hua
Zheng, Ni
Gao, Qi
Si, Yuanquan
Zhao, Yueran
author_sort Pan, Cuicui
collection PubMed
description BACKGROUND: MiR-320 is downregulated in multiple cancers, including glioma and acts as tumor suppressor through inhibiting tumor cells proliferation and inducing apoptosis. PBX3 (Pre-B cell leukemia homeobox 3), a putative target gene of miR-320, has been reported to be upregulated in various tumors and promote tumor cell growth through regulating MAKP/ERK pathway. This study aimed to verify whether miR-320 influences glioma cells growth through regulating PBX3. METHODS: Twenty-four human glioma and paired adjacent nontumorous tissues were collected for determination of miR-320 and PBX3 expression using RT-qPCR and western blot assays. Luciferase reporter assay was performed to verify the interaction between miR-320 and its targeting sequence in the 3′ UTR of PBX3 in glioma cells U87 and U251. Increased miR-320 level in U87 and U251 cells was achieved through miR-320 mimic transfection and the effect of which on glioma cells growth, proliferation, cell cycle, apoptosis and activation of Raf-1/MAPK pathway was determined using MTT, colony formation, flow cytometry and western blot assays. PBX3 knockdown was performed using shPBX3 and the influence on MAPK pathway activation was evaluated. RESULTS: MiR-320 downregulation and PBX3 upregulation was found in glioma tissues. Luciferase reporter assays identified miR-320 directly blinds to the 3′ UTR of PBX3 in glioma cells. MiR-320 mimic transfection suppressed glioma cells proliferation, and induced cell cycle arrest and apoptosis. Both miR-320 overexpression and PBX3 knockdown inhibited Raf-1/MAPK activation. CONCLUSION: MiR-320 may suppress glioma cells growth and induced apoptosis through the PBX3/Raf-1/MAPK axis, and miR-320 oligonucleotides may be a potential cancer therapeutic for glioma.
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spelling pubmed-56090342017-09-25 MiR-320 inhibits the growth of glioma cells through downregulating PBX3 Pan, Cuicui Gao, Hua Zheng, Ni Gao, Qi Si, Yuanquan Zhao, Yueran Biol Res Research Article BACKGROUND: MiR-320 is downregulated in multiple cancers, including glioma and acts as tumor suppressor through inhibiting tumor cells proliferation and inducing apoptosis. PBX3 (Pre-B cell leukemia homeobox 3), a putative target gene of miR-320, has been reported to be upregulated in various tumors and promote tumor cell growth through regulating MAKP/ERK pathway. This study aimed to verify whether miR-320 influences glioma cells growth through regulating PBX3. METHODS: Twenty-four human glioma and paired adjacent nontumorous tissues were collected for determination of miR-320 and PBX3 expression using RT-qPCR and western blot assays. Luciferase reporter assay was performed to verify the interaction between miR-320 and its targeting sequence in the 3′ UTR of PBX3 in glioma cells U87 and U251. Increased miR-320 level in U87 and U251 cells was achieved through miR-320 mimic transfection and the effect of which on glioma cells growth, proliferation, cell cycle, apoptosis and activation of Raf-1/MAPK pathway was determined using MTT, colony formation, flow cytometry and western blot assays. PBX3 knockdown was performed using shPBX3 and the influence on MAPK pathway activation was evaluated. RESULTS: MiR-320 downregulation and PBX3 upregulation was found in glioma tissues. Luciferase reporter assays identified miR-320 directly blinds to the 3′ UTR of PBX3 in glioma cells. MiR-320 mimic transfection suppressed glioma cells proliferation, and induced cell cycle arrest and apoptosis. Both miR-320 overexpression and PBX3 knockdown inhibited Raf-1/MAPK activation. CONCLUSION: MiR-320 may suppress glioma cells growth and induced apoptosis through the PBX3/Raf-1/MAPK axis, and miR-320 oligonucleotides may be a potential cancer therapeutic for glioma. BioMed Central 2017-09-21 /pmc/articles/PMC5609034/ /pubmed/28934982 http://dx.doi.org/10.1186/s40659-017-0137-4 Text en © The Author(s) 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Pan, Cuicui
Gao, Hua
Zheng, Ni
Gao, Qi
Si, Yuanquan
Zhao, Yueran
MiR-320 inhibits the growth of glioma cells through downregulating PBX3
title MiR-320 inhibits the growth of glioma cells through downregulating PBX3
title_full MiR-320 inhibits the growth of glioma cells through downregulating PBX3
title_fullStr MiR-320 inhibits the growth of glioma cells through downregulating PBX3
title_full_unstemmed MiR-320 inhibits the growth of glioma cells through downregulating PBX3
title_short MiR-320 inhibits the growth of glioma cells through downregulating PBX3
title_sort mir-320 inhibits the growth of glioma cells through downregulating pbx3
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5609034/
https://www.ncbi.nlm.nih.gov/pubmed/28934982
http://dx.doi.org/10.1186/s40659-017-0137-4
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