Nicotine Promoted Colon Cancer Growth via Epidermal Growth Factor Receptor, c-Src, and 5-Lipoxygenase-Mediated Signal Pathway

@article{Ye2004NicotinePC,
  title={Nicotine Promoted Colon Cancer Growth via Epidermal Growth Factor Receptor, c-Src, and 5-Lipoxygenase-Mediated Signal Pathway},
  author={Yi Ni Ye and Edgar S. L. Liu and Vivian Yvonne Shin and William Ka Kei Wu and Jiing‐Chyuan Luo and Chi Hin Cho},
  journal={Journal of Pharmacology and Experimental Therapeutics},
  year={2004},
  volume={308},
  pages={66 - 72}
}
  • Y. Ye, E. S. Liu, C. Cho
  • Published 1 January 2004
  • Biology, Medicine
  • Journal of Pharmacology and Experimental Therapeutics
Nicotine [3-(1-methyl-2-pyrrolidinyl)-pyridine], a major alkaloid in tobacco, has been implicated as playing a role in carcinogenesis. Our previous study showed that passive cigarette smoking promoted inflammation-associated colonic adenoma formation in mice, and 5-lipoxygenase (5-LOX) plays an important role in this process. In the present study, we aimed to investigate whether nicotine could stimulate colon cancer cell proliferation and tumor growth in nude mice xenograft model and the… 
View on ASPET
jpet.aspetjournals.org
96 Citations
Highly Influential Citations
1
Background Citations
39
Methods Citations
1
Results Citations
2

Figures and Tables from this paper

96 Citations

Citation Type

Citation Type

Nicotine promotes mammary tumor migration via a signaling cascade involving protein kinase C and CDC42.
TLDR
Investigation of the signaling pathways by which nicotine potentiates tumorigenesis in human mammary epithelial-like MCF10A or cancerous MCF7 cells suggests that nicotine, through interacting with its receptor, initiates a signaling cascade that involves PKC and cdc42 and consequently promotes migration in mammaries epithelial or tumor cells.
Cyclooxygenase-2 in cancer cells and macrophages induces colon cancer cell growth by cigarette smoke extract.
Nicotine-Mediated Cell Proliferation and Tumor Progression in Smoking-Related Cancers
TLDR
The molecular mechanisms by which nicotine and its oncogenic derivatives such as 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and N-nitrosonornicotine induce cell-cycle progression and promote tumor growth are discussed.
Nicotine Induces Cyclooxygenase-2 and Vascular Endothelial Growth Factor Receptor-2 in Association with Tumor-Associated Invasion and Angiogenesis in Gastric Cancer
TLDR
The results reveal that the promoting action of nicotine on angiogenesis, tumor invasion, and metastasis is COX-2/VEGF/VEGFR dependent.
Nicotine induces cell proliferation by beta-arrestin-mediated activation of Src and Rb-Raf-1 pathways.
TLDR
It appears that nicotine induces cell proliferation by beta-arrestin-mediated activation of the Src and Rb-Raf-1 pathways.
Nicotine increases survival in human colon cancer cells treated with chemotherapeutic drugs.
Rapid activation of Stat3 and ERK1/2 by nicotine modulates cell proliferation in human bladder cancer cells.
TLDR
It is concluded that through nAChR and beta-adrenoceptors, nicotine activates ERK1/2 and Stat3 signaling pathways, leading to Cyclin D1 expression and cell proliferation, in bladder cells.
Rapid Activation of Stat 3 and ERK 1 / 2 by Nicotine Modulates Cell Proliferation in Human Bladder Cancer Cells
TLDR
Investigating whether there is nicotine-induced bladder epithelial cell proliferation and to identify the signaling transduction pathway regulated by nicotine found that nicotine simultaneously activates Stat3 and extracellular signal regulated kinase 1/2 (ERK1/2) in T24 cells.
Dual inhibition of 5-LOX and COX-2 suppresses colon cancer formation promoted by cigarette smoke.
TLDR
Results indicate that inhibition of COX-2 may lead to a shunt of arachidonic acid metabolism towards the leukotriene pathway during colonic tumorigenesis promoted by CSE, and blocker of both COx-2 and 5-LOX may present a superior anticancer profile in cigarette smokers.
Nicotine Promotes Proliferation of Human Nasopharyngeal Carcinoma Cells by Regulating α7AChR, ERK, HIF-1α and VEGF/PEDF Signaling
TLDR
Results indicate that nicotine promotes proliferation of human NPC cells in vitro through simultaneous modulation of α7AChR, Hif-1α, ERK and VEGF/PEDF signaling and suggest that the related molecules such as HIF-1 α might be the potential therapeutic targets for tobacco-associated diseases such as nasopharyngeal carcinomas.
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 39 REFERENCES
Signalling pathways involved in nicotine regulation of apoptosis of human lung cancer cells.
TLDR
Evidence is provided that nicotine activates the mitogen-activated protein (MAP) kinase signalling pathway in lung cancer cells, specifically extracellular signal-regulated kinase (ERK2), resulting in increased expression of the bcl-2 protein and inhibition of apoptosis in these cells, and suggests caution in the use of smokeless tobacco products to treat smoking addiction.
Effect of serotonin and nicotine on the growth of a human small cell lung cancer xenograft.
TLDR
The stimulatory effect of nicotine on an SCLC tumor was not demonstrated and two dose levels of each compound, namely 20 and 200 micrograms/day, were used to investigate their effects on tumor growth.
Epidermal growth factor receptor expression in primary cultured human colorectal carcinoma cells.
TLDR
In situ hybridization on human colon tissue demonstrates that epidermal growth factor receptor (EGFR) mRNA expression is strongly increased during tumour progression, and redistribution of EGFR to apical plasma membranes in advanced colon carcinoma cells suggests that autocrine growth factors in the colon lumen may play a significant role during tumours progression.
Up‐Regulation of Epidermal Growth Factor‐Receptors (EGF‐R) by Nicotine in Cervical Cancer Cell Lines: This Effect May Be Mediated by EGF
TLDR
The data show that nicotine‐induced proliferation of cervical cancer cells is mediated through EGF‐R over‐expression and that this action of nicotine utilizes EGF.
Up-regulation of vascular endothelial growth factor by membrane-type 1 matrix metalloproteinase stimulates human glioma xenograft growth and angiogenesis.
TLDR
It is demonstrated that the enhanced tumorigenicity of glioma cells overexpressing MT1-MMP involves stimulation of angiogenesis through the up-regulation of VEGF production.
Level and function of epidermal growth factor receptor predict the metastatic potential of human colon carcinoma cells.
  • R. Radinsky, S. Risin, I. Fidler
  • Biology, Medicine
    Clinical cancer research : an official journal of the American Association for Cancer Research
  • 1995
TLDR
It is demonstrated that expression of EGF-R by HCC cells directly correlates with their ability to produce hepatic metastasis, and that only cells with high expression of the epidermal growth factor receptor produced a high incidence of liver metastasis.
Nicotine‐induced phosphorylation of Akt through epidermal growth factor receptor and Src in PC12h cells
TLDR
It is suggested that nicotine induces the activation of both PI3‐kinase/Akt and ERK pathways via common pathways including non‐α7‐nAChRs, L‐type VSCC, CaM kinase II and EGFR in PC12h cells, but Src family tyrosine kinases only participate in the pathway to activate Akt.
Effects of in vivo treatments of nicotine and benzo[a]pyrene on the epidermal growth factor receptor in hamster buccal pouch.
Nicotine stimulates a serotonergic autocrine loop in human small-cell lung carcinoma.
The cyclooxygenase inhibitor ibuprofen and the FLAP inhibitor MK886 inhibit pancreatic carcinogenesis induced in hamsters by transplacental exposure to ethanol and the tobacco carcinogen NNK
TLDR
The findings suggest an important role of the AA-cascade in the genesis of this cancer type and indicate that pharmacological or dietary measures that reduce AA-metabolism may be useful for the prevention and clinical management of pancreatic cancer.
...
1
2
3
4
...