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Effects of receptor for advanced glycation endproducts on microvessel formation in endometrial cancer

BACKGROUND: The receptor for advanced glycation endproducts (RAGE) and microvascular status both play a critical role in cancer progression. However, the crosstalk between RAGE and microvascular formation in endometrial cancer remains largely unknown. METHODS: RAGE expression and microvessel density...

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Autores principales: Zheng, Lu, Li, Da, Zhou, Yi-Ming, Yang, Hui, Cheng, Di, Ma, Xiao-Xin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4751660/
https://www.ncbi.nlm.nih.gov/pubmed/26873694
http://dx.doi.org/10.1186/s12885-016-2126-3
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author Zheng, Lu
Li, Da
Zhou, Yi-Ming
Yang, Hui
Cheng, Di
Ma, Xiao-Xin
author_facet Zheng, Lu
Li, Da
Zhou, Yi-Ming
Yang, Hui
Cheng, Di
Ma, Xiao-Xin
author_sort Zheng, Lu
collection PubMed
description BACKGROUND: The receptor for advanced glycation endproducts (RAGE) and microvascular status both play a critical role in cancer progression. However, the crosstalk between RAGE and microvascular formation in endometrial cancer remains largely unknown. METHODS: RAGE expression and microvessel density were examined in 20 cases of normal endometrial tissue, 37 cases of well-differentiated endometrial cancer tissue, and 35 cases of poorly-differentiated endometrial cancer tissue. Regression analysis was used to examine the relationship between RAGE and microvessel density. The knockdown of RAGE was achieved using a small interfering RNA in HEC-1A endometrial cancer cells. A xenografted tumour model was used to evaluate RAGE-mediated microvascular formation and proliferation of endometrial cancer cells. RESULTS: It was shown that (i) RAGE expression gradually increased in normal endometrium, well-differentiated endometrial cancer, and poorly-differentiated endometrial cancer, respectively; (ii) a positive correlation existed between RAGE and microvessel density in human endometrial cancer samples; (iii) RAGE knockdown was effective in decreasing microvessel formation in xenografted tumour models; and (iv) RAGE knockdown can significantly inhibit the proliferation of endometrial cancer cells in vivo. CONCLUSIONS: These results indicate that RAGE may be a potential trigger in microvascular formation and proliferation in the development of endometrial cancer. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12885-016-2126-3) contains supplementary material, which is available to authorized users.
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spelling pubmed-47516602016-02-13 Effects of receptor for advanced glycation endproducts on microvessel formation in endometrial cancer Zheng, Lu Li, Da Zhou, Yi-Ming Yang, Hui Cheng, Di Ma, Xiao-Xin BMC Cancer Research Article BACKGROUND: The receptor for advanced glycation endproducts (RAGE) and microvascular status both play a critical role in cancer progression. However, the crosstalk between RAGE and microvascular formation in endometrial cancer remains largely unknown. METHODS: RAGE expression and microvessel density were examined in 20 cases of normal endometrial tissue, 37 cases of well-differentiated endometrial cancer tissue, and 35 cases of poorly-differentiated endometrial cancer tissue. Regression analysis was used to examine the relationship between RAGE and microvessel density. The knockdown of RAGE was achieved using a small interfering RNA in HEC-1A endometrial cancer cells. A xenografted tumour model was used to evaluate RAGE-mediated microvascular formation and proliferation of endometrial cancer cells. RESULTS: It was shown that (i) RAGE expression gradually increased in normal endometrium, well-differentiated endometrial cancer, and poorly-differentiated endometrial cancer, respectively; (ii) a positive correlation existed between RAGE and microvessel density in human endometrial cancer samples; (iii) RAGE knockdown was effective in decreasing microvessel formation in xenografted tumour models; and (iv) RAGE knockdown can significantly inhibit the proliferation of endometrial cancer cells in vivo. CONCLUSIONS: These results indicate that RAGE may be a potential trigger in microvascular formation and proliferation in the development of endometrial cancer. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12885-016-2126-3) contains supplementary material, which is available to authorized users. BioMed Central 2016-02-12 /pmc/articles/PMC4751660/ /pubmed/26873694 http://dx.doi.org/10.1186/s12885-016-2126-3 Text en © Zheng et al. 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Zheng, Lu
Li, Da
Zhou, Yi-Ming
Yang, Hui
Cheng, Di
Ma, Xiao-Xin
Effects of receptor for advanced glycation endproducts on microvessel formation in endometrial cancer
title Effects of receptor for advanced glycation endproducts on microvessel formation in endometrial cancer
title_full Effects of receptor for advanced glycation endproducts on microvessel formation in endometrial cancer
title_fullStr Effects of receptor for advanced glycation endproducts on microvessel formation in endometrial cancer
title_full_unstemmed Effects of receptor for advanced glycation endproducts on microvessel formation in endometrial cancer
title_short Effects of receptor for advanced glycation endproducts on microvessel formation in endometrial cancer
title_sort effects of receptor for advanced glycation endproducts on microvessel formation in endometrial cancer
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4751660/
https://www.ncbi.nlm.nih.gov/pubmed/26873694
http://dx.doi.org/10.1186/s12885-016-2126-3
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