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Effect of inhibition proliferation in human lung adenocarcinoma A549 cells by cytokine-induced killer cells
BACKGROUND: Adenocarcinoma, the most common form of lung cancer, is one of main human malignant tumors. In this paper, we focus on the effect of antitumor activity of cytokine-induced killer (CIK) cells on human lung adenocarcinoma cell line A549. METHODS: CIK cells were obtained by inducing periphe...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley & Sons, Ltd
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4511324/ https://www.ncbi.nlm.nih.gov/pubmed/26273401 http://dx.doi.org/10.1111/1759-7714.12205 |
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author | Li, Dengrui Guo, Sumin Li, Hui Zhu, Guiyun Gao, Li Xin, Xin Yan, Dandan Li, Xiuwu Geng, Shujun Hou, Hongwei Yang, Yonghui |
author_facet | Li, Dengrui Guo, Sumin Li, Hui Zhu, Guiyun Gao, Li Xin, Xin Yan, Dandan Li, Xiuwu Geng, Shujun Hou, Hongwei Yang, Yonghui |
author_sort | Li, Dengrui |
collection | PubMed |
description | BACKGROUND: Adenocarcinoma, the most common form of lung cancer, is one of main human malignant tumors. In this paper, we focus on the effect of antitumor activity of cytokine-induced killer (CIK) cells on human lung adenocarcinoma cell line A549. METHODS: CIK cells were obtained by inducing peripheral blood mononuclear cells with recombinant human (rh) interferon-gamma, monoclonal anti-CD3 antibody, rh interleukin (IL)-1alpha, and rhIL-2, which were added into the culture. A549 cell viability of CIK cells was determined using MTS assay. Flow cytometry (FCM) experiments were performed to detect cell cycle changes. The expression of P27 in A549 cells treated by CIK cells was evaluated by Western blot. RESULT: The percentage of CD3+CD16+CD56+ T cells in a representative peripheral blood mononucleated cell sample was 33.7 ± 1.3%. CIK cells, in dose and time dependent manners, inhibited the proliferation of A549. FCM demonstrated that A549 cells were accumulated in G2/M and G(0)/G(1) phases when treated with CIK cells. FCM was used to analyze whether A549 cells treated with CIK cells induced apotosis or necrosis at 10:1 or 20:1. Compared to the control group, P27 was prominently upregulated in the CIK treated group. CONCLUSION: We propose that the pharmacological mechanisms of A549 cells inhibited by CIK cells can be estimated to possibly elicit different biological significance, which, in part, can be ascribed to a different mass transport rate in vitro. |
format | Online Article Text |
id | pubmed-4511324 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | John Wiley & Sons, Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-45113242015-08-13 Effect of inhibition proliferation in human lung adenocarcinoma A549 cells by cytokine-induced killer cells Li, Dengrui Guo, Sumin Li, Hui Zhu, Guiyun Gao, Li Xin, Xin Yan, Dandan Li, Xiuwu Geng, Shujun Hou, Hongwei Yang, Yonghui Thorac Cancer Original Articles BACKGROUND: Adenocarcinoma, the most common form of lung cancer, is one of main human malignant tumors. In this paper, we focus on the effect of antitumor activity of cytokine-induced killer (CIK) cells on human lung adenocarcinoma cell line A549. METHODS: CIK cells were obtained by inducing peripheral blood mononuclear cells with recombinant human (rh) interferon-gamma, monoclonal anti-CD3 antibody, rh interleukin (IL)-1alpha, and rhIL-2, which were added into the culture. A549 cell viability of CIK cells was determined using MTS assay. Flow cytometry (FCM) experiments were performed to detect cell cycle changes. The expression of P27 in A549 cells treated by CIK cells was evaluated by Western blot. RESULT: The percentage of CD3+CD16+CD56+ T cells in a representative peripheral blood mononucleated cell sample was 33.7 ± 1.3%. CIK cells, in dose and time dependent manners, inhibited the proliferation of A549. FCM demonstrated that A549 cells were accumulated in G2/M and G(0)/G(1) phases when treated with CIK cells. FCM was used to analyze whether A549 cells treated with CIK cells induced apotosis or necrosis at 10:1 or 20:1. Compared to the control group, P27 was prominently upregulated in the CIK treated group. CONCLUSION: We propose that the pharmacological mechanisms of A549 cells inhibited by CIK cells can be estimated to possibly elicit different biological significance, which, in part, can be ascribed to a different mass transport rate in vitro. John Wiley & Sons, Ltd 2015-07 2014-12-29 /pmc/articles/PMC4511324/ /pubmed/26273401 http://dx.doi.org/10.1111/1759-7714.12205 Text en © 2014 The Authors. Thoracic Cancer published by Tianjin Lung Cancer Institute and Wiley Publishing Asia Pty Ltd. http://creativecommons.org/licenses/by-nc/4.0/ This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. |
spellingShingle | Original Articles Li, Dengrui Guo, Sumin Li, Hui Zhu, Guiyun Gao, Li Xin, Xin Yan, Dandan Li, Xiuwu Geng, Shujun Hou, Hongwei Yang, Yonghui Effect of inhibition proliferation in human lung adenocarcinoma A549 cells by cytokine-induced killer cells |
title | Effect of inhibition proliferation in human lung adenocarcinoma A549 cells by cytokine-induced killer cells |
title_full | Effect of inhibition proliferation in human lung adenocarcinoma A549 cells by cytokine-induced killer cells |
title_fullStr | Effect of inhibition proliferation in human lung adenocarcinoma A549 cells by cytokine-induced killer cells |
title_full_unstemmed | Effect of inhibition proliferation in human lung adenocarcinoma A549 cells by cytokine-induced killer cells |
title_short | Effect of inhibition proliferation in human lung adenocarcinoma A549 cells by cytokine-induced killer cells |
title_sort | effect of inhibition proliferation in human lung adenocarcinoma a549 cells by cytokine-induced killer cells |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4511324/ https://www.ncbi.nlm.nih.gov/pubmed/26273401 http://dx.doi.org/10.1111/1759-7714.12205 |
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