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Long non-coding RNA PTENP1 inhibits proliferation and migration of breast cancer cells via AKT and MAPK signaling pathways

We aimed to investigate the influence of long non-coding RNA (lncRNA) PTEN pseudogene-1 (PTENP1) on the proliferation, migration and cycle of breast cancer cells and its mechanism. Lentiviral vectors expressing PTENP1 were synthesized and breast cancer cells MCF7 were transfected with LV003-GFP-PTEN...

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Autores principales: Chen, Sheng, Wang, Ye, Zhang, Jian-Hua, Xia, Qi-Jun, Sun, Qiang, Li, Zhen-Kai, Zhang, Jian-Guo, Tang, Mao-Sheng, Dong, Mao-Sheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5649540/
https://www.ncbi.nlm.nih.gov/pubmed/29085464
http://dx.doi.org/10.3892/ol.2017.6823
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author Chen, Sheng
Wang, Ye
Zhang, Jian-Hua
Xia, Qi-Jun
Sun, Qiang
Li, Zhen-Kai
Zhang, Jian-Guo
Tang, Mao-Sheng
Dong, Mao-Sheng
author_facet Chen, Sheng
Wang, Ye
Zhang, Jian-Hua
Xia, Qi-Jun
Sun, Qiang
Li, Zhen-Kai
Zhang, Jian-Guo
Tang, Mao-Sheng
Dong, Mao-Sheng
author_sort Chen, Sheng
collection PubMed
description We aimed to investigate the influence of long non-coding RNA (lncRNA) PTEN pseudogene-1 (PTENP1) on the proliferation, migration and cycle of breast cancer cells and its mechanism. Lentiviral vectors expressing PTENP1 were synthesized and breast cancer cells MCF7 were transfected with LV003-GFP-PTENP1 and LV003-GFP, respectively. The proliferation capacities of breast cancer cells were detected using CCK-8 assay, and the migration capacities of breast cancer cells were detected using scratch assay; flow cytometry was used to detect the cell cycles and Western blot was used to detect the expression levels of cyclin A2, CDK2, p-p44/42 MAPK, t-p44/42 MAPK, p-p38 MAPK, t-p38 MAPK, p-AKT, t-AKT in AKT and MAPK pathways. The absorbance values (A450) of cells in experimental group at 48 and 72 h were 1.4±0.3 and 2.3±0.47, respectively, which were significantly lower than those in control group (3.2±0.39, 3.4±0.58) (P<0.05). The number of cell colonies in experimental group was (48±13), which was significantly lower than that in control group (159±16) (P<0.01). The cell migration rate in experimental group was 22.8±3.3%, which was significantly lower than that in control group 61.8±5.2% (P<0.01). Western blot detection showed that the expression levels of cyclin A2, CDK2, p-AKT, p-p44/42 MAPK and p-p38 MAPK in experimental group were significantly decreased compared with those in control group. LncRNA PTENP1 can inhibit the proliferation and migration of breast cancer cells via the AKT and MAPK signaling pathways.
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spelling pubmed-56495402017-10-30 Long non-coding RNA PTENP1 inhibits proliferation and migration of breast cancer cells via AKT and MAPK signaling pathways Chen, Sheng Wang, Ye Zhang, Jian-Hua Xia, Qi-Jun Sun, Qiang Li, Zhen-Kai Zhang, Jian-Guo Tang, Mao-Sheng Dong, Mao-Sheng Oncol Lett Articles We aimed to investigate the influence of long non-coding RNA (lncRNA) PTEN pseudogene-1 (PTENP1) on the proliferation, migration and cycle of breast cancer cells and its mechanism. Lentiviral vectors expressing PTENP1 were synthesized and breast cancer cells MCF7 were transfected with LV003-GFP-PTENP1 and LV003-GFP, respectively. The proliferation capacities of breast cancer cells were detected using CCK-8 assay, and the migration capacities of breast cancer cells were detected using scratch assay; flow cytometry was used to detect the cell cycles and Western blot was used to detect the expression levels of cyclin A2, CDK2, p-p44/42 MAPK, t-p44/42 MAPK, p-p38 MAPK, t-p38 MAPK, p-AKT, t-AKT in AKT and MAPK pathways. The absorbance values (A450) of cells in experimental group at 48 and 72 h were 1.4±0.3 and 2.3±0.47, respectively, which were significantly lower than those in control group (3.2±0.39, 3.4±0.58) (P<0.05). The number of cell colonies in experimental group was (48±13), which was significantly lower than that in control group (159±16) (P<0.01). The cell migration rate in experimental group was 22.8±3.3%, which was significantly lower than that in control group 61.8±5.2% (P<0.01). Western blot detection showed that the expression levels of cyclin A2, CDK2, p-AKT, p-p44/42 MAPK and p-p38 MAPK in experimental group were significantly decreased compared with those in control group. LncRNA PTENP1 can inhibit the proliferation and migration of breast cancer cells via the AKT and MAPK signaling pathways. D.A. Spandidos 2017-10 2017-08-24 /pmc/articles/PMC5649540/ /pubmed/29085464 http://dx.doi.org/10.3892/ol.2017.6823 Text en Copyright: © Chen 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
Chen, Sheng
Wang, Ye
Zhang, Jian-Hua
Xia, Qi-Jun
Sun, Qiang
Li, Zhen-Kai
Zhang, Jian-Guo
Tang, Mao-Sheng
Dong, Mao-Sheng
Long non-coding RNA PTENP1 inhibits proliferation and migration of breast cancer cells via AKT and MAPK signaling pathways
title Long non-coding RNA PTENP1 inhibits proliferation and migration of breast cancer cells via AKT and MAPK signaling pathways
title_full Long non-coding RNA PTENP1 inhibits proliferation and migration of breast cancer cells via AKT and MAPK signaling pathways
title_fullStr Long non-coding RNA PTENP1 inhibits proliferation and migration of breast cancer cells via AKT and MAPK signaling pathways
title_full_unstemmed Long non-coding RNA PTENP1 inhibits proliferation and migration of breast cancer cells via AKT and MAPK signaling pathways
title_short Long non-coding RNA PTENP1 inhibits proliferation and migration of breast cancer cells via AKT and MAPK signaling pathways
title_sort long non-coding rna ptenp1 inhibits proliferation and migration of breast cancer cells via akt and mapk signaling pathways
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5649540/
https://www.ncbi.nlm.nih.gov/pubmed/29085464
http://dx.doi.org/10.3892/ol.2017.6823
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