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Inhibitory effect of carboplatin in combination with bevacizumab on human retinoblastoma in an in vitro and in vivo model
Retinoblastoma is the most common type of malignant intraocular tumor in children, and angiogenesis is required for tumor growth and expansion. The present study investigated whether use of the vascular endothelial growth factor inhibitor antibody bevacizumab can increase the inhibitory effect of ca...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5652222/ https://www.ncbi.nlm.nih.gov/pubmed/29098028 http://dx.doi.org/10.3892/ol.2017.6827 |
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author | Zhang, Qi Cheng, Yong Huang, Lvzhen Bai, Yujing Liang, Jianhong Li, Xiaoxin |
author_facet | Zhang, Qi Cheng, Yong Huang, Lvzhen Bai, Yujing Liang, Jianhong Li, Xiaoxin |
author_sort | Zhang, Qi |
collection | PubMed |
description | Retinoblastoma is the most common type of malignant intraocular tumor in children, and angiogenesis is required for tumor growth and expansion. The present study investigated whether use of the vascular endothelial growth factor inhibitor antibody bevacizumab can increase the inhibitory effect of carboplatin on human retinoblastoma Y79 cells. This was investigated using in vitro and in vivo models. Cell proliferation was assayed using a Cell Counting Kit-8 assay, which tested different concentrations of carboplatin in combination with bevacizumab. Cell apoptosis and cell cycle were analyzed using flow cytometry. Protein levels of related signaling pathway molecules were determined by western blotting. The present study used an intravitreal retinoblastoma mouse model for the in vivo study (n=40). Tumors were analyzed histologically. The present study revealed that combining bevacizumab and carboplatin in an in vitro culture of Y79 cells led to a higher inhibition of cellular proliferation than carboplatin alone (P<0.05). The drug combination caused increased apoptosis, and a greater inhibition of the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) and mitogen activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathways. This combination also effectively inhibited tumor growth in vivo (P<0.05). These results demonstrate that a combination of carboplatin and bevacizumab results in a greater antitumor effect in advanced human retinoblastoma in vitro and in vivo by inhibiting the PI3K/Akt and MAPK/ERK pathways. |
format | Online Article Text |
id | pubmed-5652222 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-56522222017-11-02 Inhibitory effect of carboplatin in combination with bevacizumab on human retinoblastoma in an in vitro and in vivo model Zhang, Qi Cheng, Yong Huang, Lvzhen Bai, Yujing Liang, Jianhong Li, Xiaoxin Oncol Lett Articles Retinoblastoma is the most common type of malignant intraocular tumor in children, and angiogenesis is required for tumor growth and expansion. The present study investigated whether use of the vascular endothelial growth factor inhibitor antibody bevacizumab can increase the inhibitory effect of carboplatin on human retinoblastoma Y79 cells. This was investigated using in vitro and in vivo models. Cell proliferation was assayed using a Cell Counting Kit-8 assay, which tested different concentrations of carboplatin in combination with bevacizumab. Cell apoptosis and cell cycle were analyzed using flow cytometry. Protein levels of related signaling pathway molecules were determined by western blotting. The present study used an intravitreal retinoblastoma mouse model for the in vivo study (n=40). Tumors were analyzed histologically. The present study revealed that combining bevacizumab and carboplatin in an in vitro culture of Y79 cells led to a higher inhibition of cellular proliferation than carboplatin alone (P<0.05). The drug combination caused increased apoptosis, and a greater inhibition of the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) and mitogen activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathways. This combination also effectively inhibited tumor growth in vivo (P<0.05). These results demonstrate that a combination of carboplatin and bevacizumab results in a greater antitumor effect in advanced human retinoblastoma in vitro and in vivo by inhibiting the PI3K/Akt and MAPK/ERK pathways. D.A. Spandidos 2017-11 2017-08-25 /pmc/articles/PMC5652222/ /pubmed/29098028 http://dx.doi.org/10.3892/ol.2017.6827 Text en Copyright: © Zhang 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 Zhang, Qi Cheng, Yong Huang, Lvzhen Bai, Yujing Liang, Jianhong Li, Xiaoxin Inhibitory effect of carboplatin in combination with bevacizumab on human retinoblastoma in an in vitro and in vivo model |
title | Inhibitory effect of carboplatin in combination with bevacizumab on human retinoblastoma in an in vitro and in vivo model |
title_full | Inhibitory effect of carboplatin in combination with bevacizumab on human retinoblastoma in an in vitro and in vivo model |
title_fullStr | Inhibitory effect of carboplatin in combination with bevacizumab on human retinoblastoma in an in vitro and in vivo model |
title_full_unstemmed | Inhibitory effect of carboplatin in combination with bevacizumab on human retinoblastoma in an in vitro and in vivo model |
title_short | Inhibitory effect of carboplatin in combination with bevacizumab on human retinoblastoma in an in vitro and in vivo model |
title_sort | inhibitory effect of carboplatin in combination with bevacizumab on human retinoblastoma in an in vitro and in vivo model |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5652222/ https://www.ncbi.nlm.nih.gov/pubmed/29098028 http://dx.doi.org/10.3892/ol.2017.6827 |
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