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Silencing of phosphoglucose isomerase/autocrine motility factor decreases U87 human glioblastoma cell migration
Phosphoglucose isomerase/autocrine motility factor (PGI/AMF) is secreted by tumors and influences tumor growth and metastasis. In order to investigate the effects of silencing PGI/AMF on the migration and the sphere forming abilities of human glioblastoma U87 cells, as well as on the side population...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4790702/ https://www.ncbi.nlm.nih.gov/pubmed/26936801 http://dx.doi.org/10.3892/ijmm.2016.2500 |
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author | LI, YANG WEI, ZHENQING DONG, BIN LIAN, ZHIGANG XU, YINGHUI |
author_facet | LI, YANG WEI, ZHENQING DONG, BIN LIAN, ZHIGANG XU, YINGHUI |
author_sort | LI, YANG |
collection | PubMed |
description | Phosphoglucose isomerase/autocrine motility factor (PGI/AMF) is secreted by tumors and influences tumor growth and metastasis. In order to investigate the effects of silencing PGI/AMF on the migration and the sphere forming abilities of human glioblastoma U87 cells, as well as on the side population cells (SPCs), PGI/AMF was silenced using siRNA. Western blot analysis and RT-qPCR were used to assess the expression of PGI/AMF, Akt and SRY (sex determining region Y)-box 2 (SOX2). Wound healing, migration and tumorsphere formation assays were performed to assess invasion and metastatic potential. The proportion of SPCs was determined using Hoechst 33342 dye and flow cytometric analysis. PGI/AMF silencing inhibited the wound healing capacity and migration ability of U87 cells by 52.6 and 80.4%, respectively, compared with the scrambled siRNA (both P<0.001). Silencing of PGI/AMF decreased the proportion of SPCs in the U87 cells by 80.9% (P<0.01). The silencing of PGI/AMF decreased the number and size of tumorspheres by 53.1 and 39.9%, respectively, compared with the scrambled siRNA (both P<0.01). The silencing of PGI/AMF decreased the levels of phosphorylated Akt (−71.9%, P<0.001) compared with the scrambled siRNA, as well as the levels of the stemness marker, SOX2 (−61.7%, P<0.01). Taken together, these findings suggest that PGI/AMF silencing decreases migration, tumorsphere formation as well as the proportion of SPCs in glioblastoma U87 cells. We suggest that the Akt pathway is involved, and our results provide a potential new target for the treatment of glioblastoma. |
format | Online Article Text |
id | pubmed-4790702 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-47907022016-03-18 Silencing of phosphoglucose isomerase/autocrine motility factor decreases U87 human glioblastoma cell migration LI, YANG WEI, ZHENQING DONG, BIN LIAN, ZHIGANG XU, YINGHUI Int J Mol Med Articles Phosphoglucose isomerase/autocrine motility factor (PGI/AMF) is secreted by tumors and influences tumor growth and metastasis. In order to investigate the effects of silencing PGI/AMF on the migration and the sphere forming abilities of human glioblastoma U87 cells, as well as on the side population cells (SPCs), PGI/AMF was silenced using siRNA. Western blot analysis and RT-qPCR were used to assess the expression of PGI/AMF, Akt and SRY (sex determining region Y)-box 2 (SOX2). Wound healing, migration and tumorsphere formation assays were performed to assess invasion and metastatic potential. The proportion of SPCs was determined using Hoechst 33342 dye and flow cytometric analysis. PGI/AMF silencing inhibited the wound healing capacity and migration ability of U87 cells by 52.6 and 80.4%, respectively, compared with the scrambled siRNA (both P<0.001). Silencing of PGI/AMF decreased the proportion of SPCs in the U87 cells by 80.9% (P<0.01). The silencing of PGI/AMF decreased the number and size of tumorspheres by 53.1 and 39.9%, respectively, compared with the scrambled siRNA (both P<0.01). The silencing of PGI/AMF decreased the levels of phosphorylated Akt (−71.9%, P<0.001) compared with the scrambled siRNA, as well as the levels of the stemness marker, SOX2 (−61.7%, P<0.01). Taken together, these findings suggest that PGI/AMF silencing decreases migration, tumorsphere formation as well as the proportion of SPCs in glioblastoma U87 cells. We suggest that the Akt pathway is involved, and our results provide a potential new target for the treatment of glioblastoma. D.A. Spandidos 2016-04 2016-02-23 /pmc/articles/PMC4790702/ /pubmed/26936801 http://dx.doi.org/10.3892/ijmm.2016.2500 Text en Copyright: © Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles LI, YANG WEI, ZHENQING DONG, BIN LIAN, ZHIGANG XU, YINGHUI Silencing of phosphoglucose isomerase/autocrine motility factor decreases U87 human glioblastoma cell migration |
title | Silencing of phosphoglucose isomerase/autocrine motility factor decreases U87 human glioblastoma cell migration |
title_full | Silencing of phosphoglucose isomerase/autocrine motility factor decreases U87 human glioblastoma cell migration |
title_fullStr | Silencing of phosphoglucose isomerase/autocrine motility factor decreases U87 human glioblastoma cell migration |
title_full_unstemmed | Silencing of phosphoglucose isomerase/autocrine motility factor decreases U87 human glioblastoma cell migration |
title_short | Silencing of phosphoglucose isomerase/autocrine motility factor decreases U87 human glioblastoma cell migration |
title_sort | silencing of phosphoglucose isomerase/autocrine motility factor decreases u87 human glioblastoma cell migration |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4790702/ https://www.ncbi.nlm.nih.gov/pubmed/26936801 http://dx.doi.org/10.3892/ijmm.2016.2500 |
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