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RNAi targeting CXCR4 inhibits proliferation and invasion of esophageal carcinoma cells

CXC chemokine receptor 4 was found to be expressed by many different types of human cancers and its expression has been correlated with tumor aggressiveness, poor prognosis and resistance to chemotherapy. However the effect of CXCR4 on the esophageal carcinoma cells remains unclear, the present stud...

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Autores principales: Wang, Tao, Mi, Yanfang, Pian, Linping, Gao, Ping, Xu, Hong, Zheng, Yuling, Xuan, Xiaoyan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3751032/
https://www.ncbi.nlm.nih.gov/pubmed/23800042
http://dx.doi.org/10.1186/1746-1596-8-104
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author Wang, Tao
Mi, Yanfang
Pian, Linping
Gao, Ping
Xu, Hong
Zheng, Yuling
Xuan, Xiaoyan
author_facet Wang, Tao
Mi, Yanfang
Pian, Linping
Gao, Ping
Xu, Hong
Zheng, Yuling
Xuan, Xiaoyan
author_sort Wang, Tao
collection PubMed
description CXC chemokine receptor 4 was found to be expressed by many different types of human cancers and its expression has been correlated with tumor aggressiveness, poor prognosis and resistance to chemotherapy. However the effect of CXCR4 on the esophageal carcinoma cells remains unclear, the present study explored the effects of CXCR4 siRNA on proliferation and invasion of esophageal carcinoma KYSE-150 and TE-13 cells. Two siRNA sequence targeting CXCR4 gene were constructed and then were transfected into KYSE-150 and TE-13 cells by Lipofectamine™2000. Changes of CXCR4 mRNA and protein were analyzed by qRT-PCR and Western blot. Effect of CXCR4 siRNA on KYSE-150 and TE-13 cells proliferation was determined by MTT. Transwell invasion assay was used to evaluate the invasion and metastasis of KYSE-150 and TE-13 cells. Tumor growth was assessed by subcutaneous inoculation of cells into BALB/c nude mice. qRT-PCR and Western blot demonstrate that the expression level of CXCR4 gene were obviously decreased in KYSE-150 and TE-13 cells transfected with CXCR4 targeting siRNA expression vectors. The average amount of cells transfected with CXCR4 siRNA penetrating Matrigel was significantly decreased (p<0.05). Injection of CXCR4 siRNA transfected cells inhibited tumor growth in a xenograft model compared with blank and negative control groups (p <0.05). CXCR4 silenced by siRNA could suppress the proliferation, invasion and metastasis of esophageal carcinoma cell lines KYSE-150 and TE-13 in vitro and in vivo. The results provide a theoretical and experimental basis for the gene therapy of ESCC using RNAi technology based on CXCR4 target site. VIRTUAL SLIDES: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/3502376691001138
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spelling pubmed-37510322013-08-24 RNAi targeting CXCR4 inhibits proliferation and invasion of esophageal carcinoma cells Wang, Tao Mi, Yanfang Pian, Linping Gao, Ping Xu, Hong Zheng, Yuling Xuan, Xiaoyan Diagn Pathol Research CXC chemokine receptor 4 was found to be expressed by many different types of human cancers and its expression has been correlated with tumor aggressiveness, poor prognosis and resistance to chemotherapy. However the effect of CXCR4 on the esophageal carcinoma cells remains unclear, the present study explored the effects of CXCR4 siRNA on proliferation and invasion of esophageal carcinoma KYSE-150 and TE-13 cells. Two siRNA sequence targeting CXCR4 gene were constructed and then were transfected into KYSE-150 and TE-13 cells by Lipofectamine™2000. Changes of CXCR4 mRNA and protein were analyzed by qRT-PCR and Western blot. Effect of CXCR4 siRNA on KYSE-150 and TE-13 cells proliferation was determined by MTT. Transwell invasion assay was used to evaluate the invasion and metastasis of KYSE-150 and TE-13 cells. Tumor growth was assessed by subcutaneous inoculation of cells into BALB/c nude mice. qRT-PCR and Western blot demonstrate that the expression level of CXCR4 gene were obviously decreased in KYSE-150 and TE-13 cells transfected with CXCR4 targeting siRNA expression vectors. The average amount of cells transfected with CXCR4 siRNA penetrating Matrigel was significantly decreased (p<0.05). Injection of CXCR4 siRNA transfected cells inhibited tumor growth in a xenograft model compared with blank and negative control groups (p <0.05). CXCR4 silenced by siRNA could suppress the proliferation, invasion and metastasis of esophageal carcinoma cell lines KYSE-150 and TE-13 in vitro and in vivo. The results provide a theoretical and experimental basis for the gene therapy of ESCC using RNAi technology based on CXCR4 target site. VIRTUAL SLIDES: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/3502376691001138 BioMed Central 2013-06-24 /pmc/articles/PMC3751032/ /pubmed/23800042 http://dx.doi.org/10.1186/1746-1596-8-104 Text en Copyright © 2013 Wang et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Wang, Tao
Mi, Yanfang
Pian, Linping
Gao, Ping
Xu, Hong
Zheng, Yuling
Xuan, Xiaoyan
RNAi targeting CXCR4 inhibits proliferation and invasion of esophageal carcinoma cells
title RNAi targeting CXCR4 inhibits proliferation and invasion of esophageal carcinoma cells
title_full RNAi targeting CXCR4 inhibits proliferation and invasion of esophageal carcinoma cells
title_fullStr RNAi targeting CXCR4 inhibits proliferation and invasion of esophageal carcinoma cells
title_full_unstemmed RNAi targeting CXCR4 inhibits proliferation and invasion of esophageal carcinoma cells
title_short RNAi targeting CXCR4 inhibits proliferation and invasion of esophageal carcinoma cells
title_sort rnai targeting cxcr4 inhibits proliferation and invasion of esophageal carcinoma cells
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3751032/
https://www.ncbi.nlm.nih.gov/pubmed/23800042
http://dx.doi.org/10.1186/1746-1596-8-104
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