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J Cancer. 2017 Sep 16;8(16):3287-3295. doi: 10.7150/jca.19426. eCollection 2017.

Cytokine-Induced Killer Cells Modulates Resistance to Cisplatin in the A549/DDP Cell Line.

Yang L1,2,3,4,5, Du C1,2,3,4,5, Wu L1,2,3,4,5, Yu J1,2,3,4,5, An X1,2,3,4,5, Yu W1,2,3,4,5, Cao S6,2,3,4,5, Li H1,2,3,4,5, Ren X1,6,2,3,4,5.

Author information

1
Department of Immunology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China.
2
National Clinical Research Center for Cancer, Tianjin, China.
3
Key Laboratory of Cancer Immunology and Biotherapy, Tianjin, China.
4
Key Laboratory of Cancer Prevention and Therapy, Tianjin, China.
5
Tianjin's Clinical Research Center for Cancer, Tianjin, China.
6
Department of Biotherapy, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China.

Abstract

Background Cytokine-induced killer (CIK) cells can potentially enhance the tumor-killing activity of chemotherapy. Objective This study aimed to evaluate the effects of CIK cells on cisplatin (DDP) resistance in the human lung adenocarcinoma cell line A549/DDP. Methods The detect resistance index, drug resistance related-genes and cytokine secretion of A549/DDP co-cultured with CIK cells were assayed in vitro. Results After A549/DDP co-culture with CIK cells, the DDP resistance of A549/DDP significantly decreased in a time-dependent manner. The DDP resistance of A549/DDP co-cultured with CIK cells for 20 h decreased 4.93-fold compared with that of A549/DDP cells cultured alone (P<0.05). The mRNA and protein expression levels of the glutathione-S-transferase (GST) -π gene in A549/DDP significantly decreased after co-culture with CIK cells (P<0.05). The secretion of interferon (IFN)- γ significantly increased along with the co-culture time of A549/DDP with CIK cells. The expression of GST-π was restored by adding the neutralizing IFN-γ. Conclusion CIK cells can reverse the drug resistance of A549/DDP in a time-dependent manner by reducing GST-π expression to increase the accumulation of DDP. The effect of CIK cells on re-sensitizing lung cancer cells to the chemotherapy drug was partially dependent on the secretion of IFN-γ.

KEYWORDS:

GST-π; IFN-γ.; chemotherapy resistance; cytokine-induced killer cells; lung cancer

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