Cargando…

SP1 promotes tumor angiogenesis and invasion by activating VEGF expression in an acquired trastuzumab-resistant ovarian cancer model

Ovarian cancer is one of the most common gynecologic cancers and the leading cause of mortality in women worldwide. HER2/neu is overexpressed in various types of cancers and is most commonly associated with decreased survival. Trastuzumab is a humanized anti-HER2 monoclonal antibody for the treatmen...

Descripción completa

Detalles Bibliográficos
Autores principales: Su, Feng, Geng, Jing, Li, Xinying, Qiao, Chuan, Luo, Longlong, Feng, Jiannan, Dong, Xinjun, Lv, Ming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5780020/
https://www.ncbi.nlm.nih.gov/pubmed/29048687
http://dx.doi.org/10.3892/or.2017.5998
_version_ 1783294663411630080
author Su, Feng
Geng, Jing
Li, Xinying
Qiao, Chuan
Luo, Longlong
Feng, Jiannan
Dong, Xinjun
Lv, Ming
author_facet Su, Feng
Geng, Jing
Li, Xinying
Qiao, Chuan
Luo, Longlong
Feng, Jiannan
Dong, Xinjun
Lv, Ming
author_sort Su, Feng
collection PubMed
description Ovarian cancer is one of the most common gynecologic cancers and the leading cause of mortality in women worldwide. HER2/neu is overexpressed in various types of cancers and is most commonly associated with decreased survival. Trastuzumab is a humanized anti-HER2 monoclonal antibody for the treatment of HER2-positive breast cancers. However, primary and/or acquired resistance occurs in up to 62% patients during the first year of treatment. Vascular endothelial growth factor (VEGF) is a well-known angiogenesis factor involved in many physiological and pathological processes. Its significance has been implicated in promoting tumor growth and metastasis via angiogenesis. In the present study, we demonstrated that the upregulation of SP1 enhanced expression of VEGF promoting the angiogenesis and migration of trastuzumab-resistant ovarian cancer cell line SKOV3-T. Our in vitro and in vivo results both gave evidence that the SP1-VEGF axis was responsible for the enhanced malignancy, angiogenesis and migration in the acquired trastuzumab-resistant ovarian cancer cell model.
format Online
Article
Text
id pubmed-5780020
institution National Center for Biotechnology Information
language English
publishDate 2017
publisher D.A. Spandidos
record_format MEDLINE/PubMed
spelling pubmed-57800202018-02-12 SP1 promotes tumor angiogenesis and invasion by activating VEGF expression in an acquired trastuzumab-resistant ovarian cancer model Su, Feng Geng, Jing Li, Xinying Qiao, Chuan Luo, Longlong Feng, Jiannan Dong, Xinjun Lv, Ming Oncol Rep Articles Ovarian cancer is one of the most common gynecologic cancers and the leading cause of mortality in women worldwide. HER2/neu is overexpressed in various types of cancers and is most commonly associated with decreased survival. Trastuzumab is a humanized anti-HER2 monoclonal antibody for the treatment of HER2-positive breast cancers. However, primary and/or acquired resistance occurs in up to 62% patients during the first year of treatment. Vascular endothelial growth factor (VEGF) is a well-known angiogenesis factor involved in many physiological and pathological processes. Its significance has been implicated in promoting tumor growth and metastasis via angiogenesis. In the present study, we demonstrated that the upregulation of SP1 enhanced expression of VEGF promoting the angiogenesis and migration of trastuzumab-resistant ovarian cancer cell line SKOV3-T. Our in vitro and in vivo results both gave evidence that the SP1-VEGF axis was responsible for the enhanced malignancy, angiogenesis and migration in the acquired trastuzumab-resistant ovarian cancer cell model. D.A. Spandidos 2017-11 2017-09-25 /pmc/articles/PMC5780020/ /pubmed/29048687 http://dx.doi.org/10.3892/or.2017.5998 Text en Copyright: © Su 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
Su, Feng
Geng, Jing
Li, Xinying
Qiao, Chuan
Luo, Longlong
Feng, Jiannan
Dong, Xinjun
Lv, Ming
SP1 promotes tumor angiogenesis and invasion by activating VEGF expression in an acquired trastuzumab-resistant ovarian cancer model
title SP1 promotes tumor angiogenesis and invasion by activating VEGF expression in an acquired trastuzumab-resistant ovarian cancer model
title_full SP1 promotes tumor angiogenesis and invasion by activating VEGF expression in an acquired trastuzumab-resistant ovarian cancer model
title_fullStr SP1 promotes tumor angiogenesis and invasion by activating VEGF expression in an acquired trastuzumab-resistant ovarian cancer model
title_full_unstemmed SP1 promotes tumor angiogenesis and invasion by activating VEGF expression in an acquired trastuzumab-resistant ovarian cancer model
title_short SP1 promotes tumor angiogenesis and invasion by activating VEGF expression in an acquired trastuzumab-resistant ovarian cancer model
title_sort sp1 promotes tumor angiogenesis and invasion by activating vegf expression in an acquired trastuzumab-resistant ovarian cancer model
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5780020/
https://www.ncbi.nlm.nih.gov/pubmed/29048687
http://dx.doi.org/10.3892/or.2017.5998
work_keys_str_mv AT sufeng sp1promotestumorangiogenesisandinvasionbyactivatingvegfexpressioninanacquiredtrastuzumabresistantovariancancermodel
AT gengjing sp1promotestumorangiogenesisandinvasionbyactivatingvegfexpressioninanacquiredtrastuzumabresistantovariancancermodel
AT lixinying sp1promotestumorangiogenesisandinvasionbyactivatingvegfexpressioninanacquiredtrastuzumabresistantovariancancermodel
AT qiaochuan sp1promotestumorangiogenesisandinvasionbyactivatingvegfexpressioninanacquiredtrastuzumabresistantovariancancermodel
AT luolonglong sp1promotestumorangiogenesisandinvasionbyactivatingvegfexpressioninanacquiredtrastuzumabresistantovariancancermodel
AT fengjiannan sp1promotestumorangiogenesisandinvasionbyactivatingvegfexpressioninanacquiredtrastuzumabresistantovariancancermodel
AT dongxinjun sp1promotestumorangiogenesisandinvasionbyactivatingvegfexpressioninanacquiredtrastuzumabresistantovariancancermodel
AT lvming sp1promotestumorangiogenesisandinvasionbyactivatingvegfexpressioninanacquiredtrastuzumabresistantovariancancermodel