Nicotine promotes cell proliferation and induces resistance to cisplatin by α7 nicotinic acetylcholine receptor‑mediated activation in Raw264.7 and El4 cells

  • Authors:
    • Yan Yan Wang
    • Yao Liu
    • Xiao Yan Ni
    • Zhen Huan Bai
    • Qiong Yun Chen
    • Ye Zhang
    • Feng Guang Gao
  • View Affiliations

  • Published online on: December 31, 2013     https://doi.org/10.3892/or.2013.2962
  • Pages: 1480-1488
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Although nicotine is a risk factor for carcinogenesis and atherosclerosis, epidemiological data indicate that nicotine has therapeutic benefits in treating Alzheimer's disease. Our previous studies also showed that nicotine-treated dendritic cells have potential antitumor effects. Hence, the precise effects of nicotine on the biological characterizations of cells are controversial. The aim of the present study was to assess the roles of α7 nicotinic acetylcholine receptors (nAChRs), Erk1/2-p38-JNK and PI3K-Akt pathway in nicotine-mediated proliferation and anti-apoptosis effects. The results firstly showed that nicotine treatment clearly augmented cell viability and upregulated PCNA expression in both Raw264.7 and El4 cells. Meanwhile, nicotine afforded protection against cisplatin-induced toxicity through inhibiting caspase-3 activation and upregulating anti-apoptotic protein expression. Further exploration demonstrated that nicotine efficiently abolished cisplatin-promoted mitochondria translocation of Bax and the release of cytochrome c. The pretreatment of α-bungarotoxin and tubocurarine chloride significantly attenuated nicotine-augmented cell viability, abolished caspase-3 activation and α7 nAChR upregulation. Both Erk-JNK-p38 and PI3K-Akt signaling pathways could be activated by nicotine treatment in Raw264.7 and El4 cells. Notably, when Erk-JNK and PI3K-Akt activities were inhibited, nicotine-augmented cell proliferation and anti-apoptotic effects were abolished accordingly. The results presented here indicate that nicotine could achieve α7 nAChR-mediated proliferation and anti-apoptotic effects by activating Erk-JNK and PI3K-Akt pathways respectively, providing potential therapeutic molecules to deal with smoking-associated human diseases.
View Figures
View References

Related Articles

Journal Cover

2014-March
Volume 31 Issue 3

Print ISSN: 1021-335X
Online ISSN:1791-2431

Sign up for eToc alerts

Recommend to Library

The Cancer Story
Copy and paste a formatted citation
x
Spandidos Publications style
Wang YY, Liu Y, Ni XY, Bai ZH, Chen QY, Zhang Y and Gao FG: Nicotine promotes cell proliferation and induces resistance to cisplatin by α7 nicotinic acetylcholine receptor‑mediated activation in Raw264.7 and El4 cells. Oncol Rep 31: 1480-1488, 2014
APA
Wang, Y.Y., Liu, Y., Ni, X.Y., Bai, Z.H., Chen, Q.Y., Zhang, Y., & Gao, F.G. (2014). Nicotine promotes cell proliferation and induces resistance to cisplatin by α7 nicotinic acetylcholine receptor‑mediated activation in Raw264.7 and El4 cells. Oncology Reports, 31, 1480-1488. https://doi.org/10.3892/or.2013.2962
MLA
Wang, Y. Y., Liu, Y., Ni, X. Y., Bai, Z. H., Chen, Q. Y., Zhang, Y., Gao, F. G."Nicotine promotes cell proliferation and induces resistance to cisplatin by α7 nicotinic acetylcholine receptor‑mediated activation in Raw264.7 and El4 cells". Oncology Reports 31.3 (2014): 1480-1488.
Chicago
Wang, Y. Y., Liu, Y., Ni, X. Y., Bai, Z. H., Chen, Q. Y., Zhang, Y., Gao, F. G."Nicotine promotes cell proliferation and induces resistance to cisplatin by α7 nicotinic acetylcholine receptor‑mediated activation in Raw264.7 and El4 cells". Oncology Reports 31, no. 3 (2014): 1480-1488. https://doi.org/10.3892/or.2013.2962