English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Open

Presents the pdf analysis as premium feature

PDF Analysis

Insights

Presents the summarisation as premium feature

Summarisation

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

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 .

Effect of inhibition proliferation in human lung adenocarcinoma A549 cells by cytokine‐induced killer cells