search button

Cytokine-induced killer cells induce apoptosis and inhibit the Akt/nuclear factor-κB signaling pathway in cisplatin-resistant human glioma U87MG cells

  • Authors:
    • Yunpeng Cui
    • Feng Yang
    • Lu He

  • View Affiliations

  • Published online on: August 21, 2015     https://doi.org/10.3892/mmr.2015.4236
  • Pages: 7027-7032
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Despite advances in the development of treatment methods, glioma remains among the cancer types with a high rate of mortality. Therefore, significant efforts are made to develop novel strategies for the treatment of glioma. Ineffective, long-term cancer chemotherapy can lead to multidrug resistance (MDR), which is one of the most common reasons for the failure of chemotherapy. The present study investigated the effects of cytokine‑induced killer cells (CIK) on reversing MDR in cisplatin-resistant U87MG cells (U87MG/DDP). Mononuclear cells were isolated from the peripheral blood of healthy individuals and cultured in vitro in the presence of a combination of cytokines to generate CIK for the treatment of U87MG/DDP. An MTS assay, flow cytometric analysis of apoptosis, ELISA, western blotting and reverse transcription quantitative polymerase chain reaction were used to investigate the MDR-reversing effects of CIK as well as the underlying mechanisms. The results showed that cisplatin sensitivity and the apoptotic rate following cisplatin treatment were increased, P‑glycoprotein expression was decreased and the intracellular rhodamine‑123 content was increased in U87MG/DDP co‑cultured with CIK. In addition, the present study also identified increased mRNA and protein expression levels of MDR gene 1 (MDR1), MDR‑associated protein 1 (MRP1), B-cell lymphoma 2, Survivin and glutathione S-transferase‑π, while the phosphorylation of AKT and the transcriptional activity of nuclear factor‑κB in CIK co‑cultured U87MG/DDP was decreased. These results indicated that pre‑treatment with CIK reversed the MDR of U87MG/DDP, and that CIK‑induced apoptosis of U87MG/DDP was associated with the inhibition of Akt/NF‑κB. These findings suggested that treatment with CIK may be an effective method to enhance the sensitivity of patients with glioma to chemotherapy.
View Figures
View References

Related Articles

Journal Cover

November-2015
Volume 12 Issue 5

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

  • Journal Metrics
  • Impact Factor: 3.4
  • Ranked Medicine Research and Experimental
    (total number of cites)
  • CiteScore: 6.9
  • CiteScore Rank: Q2: #98/328 Biochemistry, Genetics and Molecular Biology
  • Source Normalized Impact per Paper (SNIP): 0.721
  • SCImago Journal Rank (SJR): 0.65
International Symposium on Molecular Medicine Conference Banner
The Cancer Story
World Congress on Advances in Oncology and International Symposium on Molecular Medicine Conference Banner
World Academy Of Sciences Banner
Heyday Road Banner

0

Copy and paste a formatted citation
x
Spandidos Publications style
Cui Y, Yang F and He L: Cytokine-induced killer cells induce apoptosis and inhibit the Akt/nuclear factor-κB signaling pathway in cisplatin-resistant human glioma U87MG cells. Mol Med Rep 12: 7027-7032, 2015
APA
Cui, Y., Yang, F., & He, L. (2015). Cytokine-induced killer cells induce apoptosis and inhibit the Akt/nuclear factor-κB signaling pathway in cisplatin-resistant human glioma U87MG cells. Molecular Medicine Reports, 12, 7027-7032. https://doi.org/10.3892/mmr.2015.4236
MLA
Cui, Y., Yang, F., He, L."Cytokine-induced killer cells induce apoptosis and inhibit the Akt/nuclear factor-κB signaling pathway in cisplatin-resistant human glioma U87MG cells". Molecular Medicine Reports 12.5 (2015): 7027-7032.
Chicago
Cui, Y., Yang, F., He, L."Cytokine-induced killer cells induce apoptosis and inhibit the Akt/nuclear factor-κB signaling pathway in cisplatin-resistant human glioma U87MG cells". Molecular Medicine Reports 12, no. 5 (2015): 7027-7032. https://doi.org/10.3892/mmr.2015.4236