Open AccessEffect of inhibition proliferation in human lung adenocarcinoma A549 cells by cytokine‐induced killer cells
Author(s) -
Li Dengrui,
Guo Sumin,
Li Hui,
Zhu Guiyun,
Gao Li,
Xin Xin,
Yan Dandan,
Li Xiuwu,
Geng Shujun,
Hou Hongwei,
Yang Yonghui
Publication year - 2015
Publication title -
thoracic cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.823
H-Index - 28
eISSN - 1759-7714
pISSN - 1759-7706
DOI - 10.1111/1759-7714.12205
Subject(s) - a549 cell , cytokine induced killer cell , flow cytometry , medicine , cytokine , peripheral blood mononuclear cell , apoptosis , cancer research , cell culture , cell cycle , cell , adenocarcinoma , cell growth , immunology , lung cancer , microbiology and biotechnology , cd3 , biology , in vitro , antigen , pathology , cancer , cd8 , biochemistry , genetics
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 .