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脂质体转染UCH-L1 siRNA对肺腺癌细胞系H157细胞增殖和凋亡的影响
BACKGROUND AND OBJECTIVE: Several reports demonstrated that the ubiquitin C terminal hydrolase-L1 (UCH-L1) has been found to be an oncogene in malignant tumors such as esophageal carcinoma, lung cancer and breast cancer. The aim of this study is to explore the effects of liposomal transfection of UC...
Formato: | Online Artículo Texto |
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Lenguaje: | English |
Publicado: |
中国肺癌杂志编辑部
2010
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6000435/ https://www.ncbi.nlm.nih.gov/pubmed/20677552 http://dx.doi.org/10.3779/j.issn.1009-3419.2010.04.04 |
_version_ | 1783331724183207936 |
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collection | PubMed |
description | BACKGROUND AND OBJECTIVE: Several reports demonstrated that the ubiquitin C terminal hydrolase-L1 (UCH-L1) has been found to be an oncogene in malignant tumors such as esophageal carcinoma, lung cancer and breast cancer. The aim of this study is to explore the effects of liposomal transfection of UCH-L1 siRNA on the proliferation and apoptosis of lung adenocarcinoma cell lines H157. METHODS: UCH-L1 siRNA was synthesized and transfected into H157 cell by liposome. Cell morphological change was observed with microscope, and cell proliferation and apoptosis index detected by flow cytometry, UCH-L1 mRNA expression was determined by RT-PCR and protein level of UCH-L1 was determined by Western blot. RESULTS: For the H157 cell transfected with siRNA, cell proliferation was inhibited significantly, cell apoptosis appeared obviously, the expression of UCH-L1 mRNA and protein level of UCH-L1 significantly decreased. CONCLUSION: UCH-L1 siRNA is able to inhibit the proliferation of lung adenocarcinoma cell lines H157 and induce the apoptosis. UCH-L1 might become a new target for lung carcinoma gene therapy. |
format | Online Article Text |
id | pubmed-6000435 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | 中国肺癌杂志编辑部 |
record_format | MEDLINE/PubMed |
spelling | pubmed-60004352018-07-06 脂质体转染UCH-L1 siRNA对肺腺癌细胞系H157细胞增殖和凋亡的影响 Zhongguo Fei Ai Za Zhi 基础研究 BACKGROUND AND OBJECTIVE: Several reports demonstrated that the ubiquitin C terminal hydrolase-L1 (UCH-L1) has been found to be an oncogene in malignant tumors such as esophageal carcinoma, lung cancer and breast cancer. The aim of this study is to explore the effects of liposomal transfection of UCH-L1 siRNA on the proliferation and apoptosis of lung adenocarcinoma cell lines H157. METHODS: UCH-L1 siRNA was synthesized and transfected into H157 cell by liposome. Cell morphological change was observed with microscope, and cell proliferation and apoptosis index detected by flow cytometry, UCH-L1 mRNA expression was determined by RT-PCR and protein level of UCH-L1 was determined by Western blot. RESULTS: For the H157 cell transfected with siRNA, cell proliferation was inhibited significantly, cell apoptosis appeared obviously, the expression of UCH-L1 mRNA and protein level of UCH-L1 significantly decreased. CONCLUSION: UCH-L1 siRNA is able to inhibit the proliferation of lung adenocarcinoma cell lines H157 and induce the apoptosis. UCH-L1 might become a new target for lung carcinoma gene therapy. 中国肺癌杂志编辑部 2010-04-20 /pmc/articles/PMC6000435/ /pubmed/20677552 http://dx.doi.org/10.3779/j.issn.1009-3419.2010.04.04 Text en 版权所有©《中国肺癌杂志》编辑部2010 https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 3.0) License. See: https://creativecommons.org/licenses/by/3.0/ |
spellingShingle | 基础研究 脂质体转染UCH-L1 siRNA对肺腺癌细胞系H157细胞增殖和凋亡的影响 |
title | 脂质体转染UCH-L1 siRNA对肺腺癌细胞系H157细胞增殖和凋亡的影响 |
title_full | 脂质体转染UCH-L1 siRNA对肺腺癌细胞系H157细胞增殖和凋亡的影响 |
title_fullStr | 脂质体转染UCH-L1 siRNA对肺腺癌细胞系H157细胞增殖和凋亡的影响 |
title_full_unstemmed | 脂质体转染UCH-L1 siRNA对肺腺癌细胞系H157细胞增殖和凋亡的影响 |
title_short | 脂质体转染UCH-L1 siRNA对肺腺癌细胞系H157细胞增殖和凋亡的影响 |
title_sort | 脂质体转染uch-l1 sirna对肺腺癌细胞系h157细胞增殖和凋亡的影响 |
topic | 基础研究 |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6000435/ https://www.ncbi.nlm.nih.gov/pubmed/20677552 http://dx.doi.org/10.3779/j.issn.1009-3419.2010.04.04 |
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