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Suppression of human epidermal growth factor receptor 2 via interference increases the chemosensitivity of ovarian carcinoma

The function of human epidermal growth factor receptor 2 (HER2) in the chemosensitivity of ovarian carcinoma has not been fully investigated, therefore, the present study aimed to analyze the potential role of HER2 in ovarian carcinoma chemosensitivity in further detail. SKOV3 cells were transfected...

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Autores principales: SONG, XIAOPING, SUN, KAILV, HU, JIANMING, ZHOU, JIANGHU
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4840778/
https://www.ncbi.nlm.nih.gov/pubmed/27123058
http://dx.doi.org/10.3892/ol.2016.4341
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author SONG, XIAOPING
SUN, KAILV
HU, JIANMING
ZHOU, JIANGHU
author_facet SONG, XIAOPING
SUN, KAILV
HU, JIANMING
ZHOU, JIANGHU
author_sort SONG, XIAOPING
collection PubMed
description The function of human epidermal growth factor receptor 2 (HER2) in the chemosensitivity of ovarian carcinoma has not been fully investigated, therefore, the present study aimed to analyze the potential role of HER2 in ovarian carcinoma chemosensitivity in further detail. SKOV3 cells were transfected with lentiviral-mediated HER2-small hairpin RNA (shRNA) molecules to establish the stable expression of HER2-shRNA in the SKOV3 cell line (knockdown cells; KD) and negative control cell line (NC). The untransfected SKOV3 cell line served as the blank control (CON) group. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis were used to detect the expression of HER2 in the three different cell types, which were subsequently examined for growth inhibition using a cell counting kit-8 assay. The CON and KD cell strains were utilized to establish xenograft models in nude mice, primarily to detect the expression of the HER2 protein, and additionally to observe tumor size changes under the treatment of cisplatin (DDP) chemotherapy. RT-qPCR and western blot analysis demonstrated a significant decrease in the levels of HER2 mRNA and protein in the KD cells. The suppression of HER2 expression resulted in an increase of chemotherapy sensitivity in the SKOV3 cells. HER2 protein expression decreased significantly following transduction with specific HER2-shRNA. Additionally, growth slowed significantly under treatment with DDP in ovarian cancer transplantation tumors. In conclusion, lentivirus-mediated HER2-shRNA effectively inhibits the expression of the HER2 gene, and increases the chemosensitivity to DDP in ovarian carcinoma.
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spelling pubmed-48407782016-04-27 Suppression of human epidermal growth factor receptor 2 via interference increases the chemosensitivity of ovarian carcinoma SONG, XIAOPING SUN, KAILV HU, JIANMING ZHOU, JIANGHU Oncol Lett Articles The function of human epidermal growth factor receptor 2 (HER2) in the chemosensitivity of ovarian carcinoma has not been fully investigated, therefore, the present study aimed to analyze the potential role of HER2 in ovarian carcinoma chemosensitivity in further detail. SKOV3 cells were transfected with lentiviral-mediated HER2-small hairpin RNA (shRNA) molecules to establish the stable expression of HER2-shRNA in the SKOV3 cell line (knockdown cells; KD) and negative control cell line (NC). The untransfected SKOV3 cell line served as the blank control (CON) group. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis were used to detect the expression of HER2 in the three different cell types, which were subsequently examined for growth inhibition using a cell counting kit-8 assay. The CON and KD cell strains were utilized to establish xenograft models in nude mice, primarily to detect the expression of the HER2 protein, and additionally to observe tumor size changes under the treatment of cisplatin (DDP) chemotherapy. RT-qPCR and western blot analysis demonstrated a significant decrease in the levels of HER2 mRNA and protein in the KD cells. The suppression of HER2 expression resulted in an increase of chemotherapy sensitivity in the SKOV3 cells. HER2 protein expression decreased significantly following transduction with specific HER2-shRNA. Additionally, growth slowed significantly under treatment with DDP in ovarian cancer transplantation tumors. In conclusion, lentivirus-mediated HER2-shRNA effectively inhibits the expression of the HER2 gene, and increases the chemosensitivity to DDP in ovarian carcinoma. D.A. Spandidos 2016-05 2016-03-16 /pmc/articles/PMC4840778/ /pubmed/27123058 http://dx.doi.org/10.3892/ol.2016.4341 Text en Copyright: © Song 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
SONG, XIAOPING
SUN, KAILV
HU, JIANMING
ZHOU, JIANGHU
Suppression of human epidermal growth factor receptor 2 via interference increases the chemosensitivity of ovarian carcinoma
title Suppression of human epidermal growth factor receptor 2 via interference increases the chemosensitivity of ovarian carcinoma
title_full Suppression of human epidermal growth factor receptor 2 via interference increases the chemosensitivity of ovarian carcinoma
title_fullStr Suppression of human epidermal growth factor receptor 2 via interference increases the chemosensitivity of ovarian carcinoma
title_full_unstemmed Suppression of human epidermal growth factor receptor 2 via interference increases the chemosensitivity of ovarian carcinoma
title_short Suppression of human epidermal growth factor receptor 2 via interference increases the chemosensitivity of ovarian carcinoma
title_sort suppression of human epidermal growth factor receptor 2 via interference increases the chemosensitivity of ovarian carcinoma
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4840778/
https://www.ncbi.nlm.nih.gov/pubmed/27123058
http://dx.doi.org/10.3892/ol.2016.4341
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