Silencing of long-non-coding RNA ANCR suppresses the migration and invasion of osteosarcoma cells by activating the p38MAPK signalling pathway

Abstract Background Osteosarcoma (OS) is a malignancy of the bone that has no clearly identified prognostic factors for diagnosis. In this study, we evaluated the regulatory role of long non-coding RNA (lncRNA) ANCR on the migration and invasion of OS cells as well as the possible mechanism involvin...

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Main Authors: Bo Liu, Hongyan Zhao, Lili Zhang, Xuefeng Shi
Format: Article
Language:English
Published: BMC 2019-11-01
Series:BMC Cancer
Subjects:
Online Access:http://link.springer.com/article/10.1186/s12885-019-6335-4
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author Bo Liu
Hongyan Zhao
Lili Zhang
Xuefeng Shi
author_facet Bo Liu
Hongyan Zhao
Lili Zhang
Xuefeng Shi
author_sort Bo Liu
collection DOAJ
description Abstract Background Osteosarcoma (OS) is a malignancy of the bone that has no clearly identified prognostic factors for diagnosis. In this study, we evaluated the regulatory role of long non-coding RNA (lncRNA) ANCR on the migration and invasion of OS cells as well as the possible mechanism involving the p38MAPK signalling pathway. Methods ANCR expression was determined in OS tissues and OS cell lines (MG-63, S1353, U2OS, and UMR-106) by qRT-PCR. It was observed that ANCR was down-regulated in MG-63 and U2OS cells by 48 h of siRNA-ANCR (si-ANCR) transfection. The proliferation of transfected cells was determined using the CCK-8 and the EdU assays. The migration and invasion of transfected cells were determined by the Transwell assay. The expression of E-cadherin, N-cadherin, and phosphorylated p38MAPK (p-p38MAPK) proteins was determined by Western blot. In addition, combinatorial treatment of cells with si-ANCR + SB203580 (p38MAPK inhibitor) was performed to investigate the association between ANCR and MAPK signalling in OS cells. Results ANCR was up-regulated in OS cells and tissues. ANCR silencing significantly inhibited the proliferation rate, decreased the percentage of migration and invasion cells, down-regulated N-cadherin, and up-regulated E-cadherin and p-p38MAPK in MG-63 and U2OS cells. Inhibition of the p38MAPK signalling pathway (SB203580) in MG-63 and U2OS cells rescued si-ANCR-induced inhibition of cell migration and invasion. Conclusions Silencing of ANCR inhibited the migration and invasion of OS cells through activation of the p38MAPK signalling pathway.
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spelling doaj.art-c0026b8c1d044bda82fdae0e6c2099462022-12-21T23:07:52ZengBMCBMC Cancer1471-24072019-11-011911910.1186/s12885-019-6335-4Silencing of long-non-coding RNA ANCR suppresses the migration and invasion of osteosarcoma cells by activating the p38MAPK signalling pathwayBo Liu0Hongyan Zhao1Lili Zhang2Xuefeng Shi3The Third Department of Orthopedics, The No. 4 Hospital of JinanDepartment of Community Section, The First People’s Hospital of JinanDepartment of Gynecology, The No. 4 Hospital of JinanDepartment of Orthopedic Trauma & Hand and Foot Surgery, Jinan Central Hospital Affiliated to Shandong UniversityAbstract Background Osteosarcoma (OS) is a malignancy of the bone that has no clearly identified prognostic factors for diagnosis. In this study, we evaluated the regulatory role of long non-coding RNA (lncRNA) ANCR on the migration and invasion of OS cells as well as the possible mechanism involving the p38MAPK signalling pathway. Methods ANCR expression was determined in OS tissues and OS cell lines (MG-63, S1353, U2OS, and UMR-106) by qRT-PCR. It was observed that ANCR was down-regulated in MG-63 and U2OS cells by 48 h of siRNA-ANCR (si-ANCR) transfection. The proliferation of transfected cells was determined using the CCK-8 and the EdU assays. The migration and invasion of transfected cells were determined by the Transwell assay. The expression of E-cadherin, N-cadherin, and phosphorylated p38MAPK (p-p38MAPK) proteins was determined by Western blot. In addition, combinatorial treatment of cells with si-ANCR + SB203580 (p38MAPK inhibitor) was performed to investigate the association between ANCR and MAPK signalling in OS cells. Results ANCR was up-regulated in OS cells and tissues. ANCR silencing significantly inhibited the proliferation rate, decreased the percentage of migration and invasion cells, down-regulated N-cadherin, and up-regulated E-cadherin and p-p38MAPK in MG-63 and U2OS cells. Inhibition of the p38MAPK signalling pathway (SB203580) in MG-63 and U2OS cells rescued si-ANCR-induced inhibition of cell migration and invasion. Conclusions Silencing of ANCR inhibited the migration and invasion of OS cells through activation of the p38MAPK signalling pathway.http://link.springer.com/article/10.1186/s12885-019-6335-4OsteosarcomaLong non-coding RNA ANCRp38MAPK signalling pathwayMigrationInvasion
spellingShingle Bo Liu
Hongyan Zhao
Lili Zhang
Xuefeng Shi
Silencing of long-non-coding RNA ANCR suppresses the migration and invasion of osteosarcoma cells by activating the p38MAPK signalling pathway
BMC Cancer
Osteosarcoma
Long non-coding RNA ANCR
p38MAPK signalling pathway
Migration
Invasion
title Silencing of long-non-coding RNA ANCR suppresses the migration and invasion of osteosarcoma cells by activating the p38MAPK signalling pathway
title_full Silencing of long-non-coding RNA ANCR suppresses the migration and invasion of osteosarcoma cells by activating the p38MAPK signalling pathway
title_fullStr Silencing of long-non-coding RNA ANCR suppresses the migration and invasion of osteosarcoma cells by activating the p38MAPK signalling pathway
title_full_unstemmed Silencing of long-non-coding RNA ANCR suppresses the migration and invasion of osteosarcoma cells by activating the p38MAPK signalling pathway
title_short Silencing of long-non-coding RNA ANCR suppresses the migration and invasion of osteosarcoma cells by activating the p38MAPK signalling pathway
title_sort silencing of long non coding rna ancr suppresses the migration and invasion of osteosarcoma cells by activating the p38mapk signalling pathway
topic Osteosarcoma
Long non-coding RNA ANCR
p38MAPK signalling pathway
Migration
Invasion
url http://link.springer.com/article/10.1186/s12885-019-6335-4
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