Role of acetylcholinesterase in lung cancer

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Abstract

Acetylcholinesterase (AChE) plays a key role in catalytic hydrolysis of cholinergic neurotransmitters. Intensive research has proven the involvement of this protein in novel functions, such as cell adhesion, differentiation, and proliferation. In addition, several recent studies have indicated that acetylcholinesterase is potentially a marker and regulator of apoptosis. Importantly, AChE is also a promising tumor suppressor. In this review, we briefly summarize the involvement of AChE in apoptosis and cancer, focusing on the role of AChE in lung cancer, as well as the therapeutic consideration of AChE for cancer therapy.

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Estimates of global mortality attributable to smoking in 2000.

Majid Ezzati, Alan Lopez (2003)

Smoking is a risk factor for several diseases and has been increasing in many developing countries. Our aim was to estimate global and regional mortality in 2000 caused by smoking, including an analysis of uncertainty. Following the methods of Peto and colleagues, we used lung-cancer mortality as an indirect marker for accumulated smoking risk. Never-smoker lung-cancer mortality was estimated based on the household use of coal with poor ventilation. Relative risks were taken from the American Cancer Society Cancer Prevention Study, phase II, and the retrospective proportional mortality analysis of Liu and colleagues in China. Relative risks were corrected for confounding and extrapolation to other regions. We estimated that in 2000, 4.83 (uncertainty range 3.94-5.93) million premature deaths in the world were attributable to smoking; 2.41 (1.80-3.15) million in developing countries and 2.43 (2.13-2.78) million in industrialised countries. 3.84 million of these deaths were in men. The leading causes of death from smoking were cardiovascular diseases (1.69 million deaths), chronic obstructive pulmonary disease (0.97 million deaths), and lung cancer (0.85 million deaths). Smoking was an important cause of global mortality in 2000. In view of the expected demographic and epidemiological transitions and current smoking patterns in the developing world, the health loss due to smoking will grow even larger unless effective interventions and policies that reduce smoking among men and prevent increases among women in developing countries are implemented.

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PTEN/PI3K/Akt pathway regulates the side population phenotype and ABCG2 activity in glioma tumor stem-like cells.

Anne-Marie Bleau, Dolores Hambardzumyan, Tatsuya Ozawa … (2009)

In normal brain, the side population (SP) phenotype is generated by ABC transporter activity and identifies stem cell and endothelial cell subpopulations by dye exclusion. By drug efflux, the ABCG2 transporter provides chemoresistance in stem cells and contributes to the blood brain barrier (BBB) when active in endothelial cells. We investigated the SP phenotype of mouse and human gliomas. In glioma endothelial cells, ABC transporter function is impaired, corresponding to disruption of the BBB in these tumors. By contrast, the SP phenotype is increased in nonendothelial cells that form neurospheres and are highly tumorigenic. In this cell population, Akt, but not its downstream target mTOR, regulates ABCG2 activity, and loss of PTEN increases the SP. This Akt-induced ABCG2 activation results from its transport to the plasma membrane. Temozolomide, the standard treatment of gliomas, although not an ABCG2 substrate, increases the SP in glioma cells, especially in cells missing PTEN.

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FOXO transcription factor activation by oxidative stress mediated by the small GTPase Ral and JNK.

Marieke A G Essers, Sanne Weijzen, Alida M. M. de Vries-Smits … (2004)

Forkhead transcription factors of the FOXO class are negatively regulated by PKB/c-Akt in response to insulin/IGF signalling, and are involved in regulating cell cycle progression and cell death. Here we show that, in contrast to insulin signalling, low levels of oxidative stress generated by treatment with H2O2 induce the activation of FOXO4. Upon treatment of cells with H2O2, the small GTPase Ral is activated and this results in a JNK-dependent phosphorylation of FOXO4 on threonine 447 and threonine 451. This Ral-mediated, JNK-dependent phosphorylation is involved in the nuclear translocation and transcriptional activation of FOXO4 after H2O2 treatment. In addition, we show that this signalling pathway is also employed by tumor necrosis factor alpha to activate FOXO4 transcriptional activity. FOXO members have been implicated in cellular protection against oxidative stress via the transcriptional regulation of manganese superoxide dismutase and catalase gene expression. The results reported here, therefore, outline a homeostasis mechanism for sustaining cellular reactive oxygen species that is controlled by signalling pathways that can convey both negative (PI-3K/PKB) and positive (Ras/Ral) inputs.

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Author and article information

Journal

Journal ID (nlm-ta): Thorac Cancer

Journal ID (iso-abbrev): Thorac Cancer

Journal ID (publisher-id): tca

Title: Thoracic Cancer

Publisher: John Wiley & Sons, Ltd (Chichester, UK )

ISSN (Print): 1759-7706

ISSN (Electronic): 1759-7714

Publication date (Print): July 2015

Publication date (Electronic): 20 March 2015

Volume: 6

Issue: 4

Pages: 390-398

Affiliations

[1 ]Digestive Endoscopy Center, Changhai Hospital, Second Military Medical University Shanghai, China

[2 ]School of Nursing, Second Military Medical University Shanghai, China

[3 ]Department of Nursing, Changhai Hospital, Second Military Medical University Shanghai, China

[4 ]Department of Gastroenterology, Changhai Hospital, Second Military Medical University Shanghai, China

Author notes

Correspondence Ling-Juan Zhang, Department of Nursing, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai 200433, China., Tel: +86 21 31161365, Fax: +86 21 31161365, Email: zxwht@ 123456163.com

Zhao-Shen Li, Department of Gastroenterology, Digestive Endoscopy Center, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai 200433, China., Tel: +86 21 25070552, Fax: +86 21 55620081, Email: zhaoshen-li@ 123456hotmail.com

Article

DOI: 10.1111/1759-7714.12249

PMC ID: 4511315

PubMed ID: 26273392

SO-VID: 8ea4d1e5-8fcd-4663-aed2-4bf91062689e

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This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

Role of acetylcholinesterase in lung cancer

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Karger: Oncology

Most cited references 80

Estimates of global mortality attributable to smoking in 2000.

PTEN/PI3K/Akt pathway regulates the side population phenotype and ABCG2 activity in glioma tumor stem-like cells.

FOXO transcription factor activation by oxidative stress mediated by the small GTPase Ral and JNK.

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