scholarly journals Nicotinic Acetylcholine Receptor Signaling in Tumor Growth and Metastasis

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Sandeep Singh ◽  
Smitha Pillai ◽  
Srikumar Chellappan
Keyword(s):  
Tumor Growth ◽  
Nicotinic Acetylcholine Receptors ◽  
Tobacco Smoke ◽  
Acetylcholine Receptors ◽  
Epithelial Mesenchymal Transition ◽  
Antitumor Effects ◽  
Nicotinic Acetylcholine ◽  
Mesenchymal Transition ◽  
Promote Cell Proliferation ◽  
Tumor Growth And Metastasis

Cigarette smoking is highly correlated with the onset of a variety of human cancers, and continued smoking is known to abrogate the beneficial effects of cancer therapy. While tobacco smoke contains hundreds of molecules that are known carcinogens, nicotine, the main addictive component of tobacco smoke, is not carcinogenic. At the same time, nicotine has been shown to promote cell proliferation, angiogenesis, and epithelial-mesenchymal transition, leading to enhanced tumor growth and metastasis. These effects of nicotine are mediated through the nicotinic acetylcholine receptors that are expressed on a variety of neuronal and nonneuronal cells. Specific signal transduction cascades that emanate from different nAChR subunits or subunit combinations facilitate the proliferative and prosurvival functions of nicotine. Nicotinic acetylcholine receptors appear to stimulate many downstream signaling cascades induced by growth factors and mitogens. It has been suggested that antagonists of nAChR signaling might have antitumor effects and might open new avenues for combating tobacco-related cancer. This paper examines the historical data connecting nicotine tumor progression and the recent efforts to target the nicotinic acetylcholine receptors to combat cancer.

scholarly journals Integrin α9β1 promotes malignant tumor growth and metastasis by potentiating epithelial-mesenchymal transition

Oncogene ◽  
2012 ◽  
Vol 32 (2) ◽  
pp. 141-150 ◽  
Author(s):  
S K Gupta ◽  
S Oommen ◽  
M-C Aubry ◽  
B P Williams ◽  
N E Vlahakis
Keyword(s):  
Tumor Growth ◽  
Malignant Tumor ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Tumor Growth And Metastasis

scholarly journals Migration of gastric cancer is suppressed by recombinant Newcastle disease virus (rL-RVG) via regulating α7-nicotinic acetylcholine receptors/ERK- EMT

BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Xuefeng Bu ◽  
Anwei Zhang ◽  
Zhengwei Chen ◽  
Xuanfeng Zhang ◽  
Riting Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Nicotinic Acetylcholine Receptors ◽  
Newcastle Disease ◽  
Acetylcholine Receptors ◽  
Gastric Cancer Cells ◽  
Nicotinic Acetylcholine ◽  
Mesenchymal Transition ◽  
Α7 Nachr

Abstract Background Nicotinic acetylcholine receptors (nAChRs) have been reported to be overexpressed in malignancies in humans and is associated with tumorigenesis and cell migration. In previous studies of gastric cancer, alpha7 nicotinic acetylcholine receptor (α7-nAChR) overexpression leads to epithelial-mesenchymal transition (EMT) and promotes the migration of gastric cancer cells. Recombinant avirulent LaSota strain of Newcastle disease virus (NDV) expressing the rabies virus glycoprotein (rL-RVG) may promote apoptosis of gastric cancer cells and reduces the migration of lung cancer metastasis. However, whether rL-RVG inhibits migration of gastric cancer cells and what the underlying functional mechanism is remains unknown. Methods The gastric cancer cell lines BGC and SGC were randomly divided into 3 groups: rL-RVG, NDV and Phosphate Buffered Solution (PBS) control groups. Furthermore,we adopted ACB and MLA,α7nAChR-siRNA for the overexpression and silencing of α7-nAChR.Corynoxenine was used for inhibiting the MEK-ERK pathway. Western blot, Immunofluoresce,cell proliferation assays,cell migration analyses through wound-healing assays and Transwell assays were used to explore the underlying mechanisms. A mouse xenograft model was used to investigate the effects of rL-RVG,NDV on tumor growth. Results In this study, our findings demonstrate that rL-RVG suppressed the migration of gastric cancer cells and reduced EMT via α7-nAChR in vitro. Furthermore rL-RVG decreased the phosphorylation levels of the MEK/ERK signaling pathway such as down-regulating the expression of P-MEK and P-ERK. Additionally, rL-RVG also reduced the expression level of mesenchymal markers N-cadherin and Vimentin and enhanced the expression of the epithelial marker E-cadherin. Lastly, rL-RVG inhibited nicotinic acetylcholine receptors (nAChRs) to suppress cell migration and epithelial to mesenchymal transition (EMT) in gastric cell. We also found that rL-RVG suppresses the growth of gastric cancer subcutaneous tumor cells in vivo. Conclusion rL-RVG inhibits α7-nAChR-MEK/ERK-EMT to suppress migration of gastric cancer cells.

scholarly journals MicroRNA-150 suppresses epithelial-mesenchymal transition, invasion, and metastasis in prostate cancer through the TRPM4-mediated β-catenin signaling pathway

2019 ◽  
Vol 316 (4) ◽  
pp. C463-C480 ◽  
Author(s):  
Xi Hong ◽  
Jian-Jun Yu
Keyword(s):  
Prostate Cancer ◽  
Tumor Growth ◽  
Signaling Pathway ◽  
Transient Receptor Potential ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition ◽  
Transient Receptor Potential Melastatin ◽  
Tumor Growth And Metastasis

Prostate cancer (PCa) remains one of the leading causes of cancer-related deaths among males. The aim of the current study was to investigate the ability of microRNA-150 (miR-150) targeting transient receptor potential melastatin 4 (TRPM4) to mediate epithelial-mesenchymal transition (EMT), invasion, and metastasis through the β-catenin signaling pathway in PCa. Microarray analysis was performed to identify PCa-related differentially expressed genes, after which both the mirDIP and TargetScan databases were employed in the prediction of the miRNAs regulating TRPM4. Immunohistochemistry and RT-qPCR were conducted to determine the expression pattern of miR-150 and TRPM4 in PCa. The relationship between miR-150 and TRPM4 expression was identified. By perturbing miR-150 and TRPM4 expression in PCa cells, cell proliferation, migration, invasion, cycle, and apoptosis as well as EMT markers were determined accordingly. Finally, tumor growth and metastasis were evaluated among nude mice. Higher TRPM4 expression and lower miR-150 expression and activation of the β-catenin signaling pathway as well as EMT stimulation were detected in the PCa tissues. Our results confirmed TRPM4 as a target of miR-150. Upregulation of miR-150 resulted in inactivation of the β-catenin signaling pathway. Furthermore, the upregulation of miR-150 or knockdown of TRPM4 was observed to suppress EMT, proliferation, migration, and invasion in vitro in addition to restrained tumor growth and metastasis in vivo. The evidence provided by our study highlights the involvement of miR-150 in the translational suppression of TRPM4 and the blockade of the β-catenin signaling pathway, resulting in the inhibition of PCa progression.

Sex difference in counts of α4 and α7 nicotinic acetylcholine receptors in the nasal polyps of adults with or without exposure to tobacco smoke

2018 ◽  
Vol 132 (7) ◽  
pp. 596-599
Author(s):  
B B Montaño-Velázquez ◽  
D A Lara-Sánchez ◽  
A Orozco-Sánchez ◽  
F J García-Vázquez ◽  
M R Mora-Campos ◽  
...  
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Tobacco Smoke ◽  
Acetylcholine Receptors ◽  
Nasal Polyps ◽  
Analysis Of Covariance ◽  
Endoscopic Polypectomy ◽  
Cigarette Tobacco ◽  
Gender Dimorphism ◽  
Nicotinic Acetylcholine ◽  
Α7 Nicotinic Acetylcholine Receptors

AbstractObjectiveTo assess counts of α4 and α7 nicotinic acetylcholine receptors in nasal polyps of adults with or without long-term exposure to cigarette tobacco smoke.MethodsTwenty-two patients with and 22 patients without exposure to cigarette tobacco smoke participated in the study. After endoscopic polypectomy, the fragments of the nasal polyps were analysed by immunohistochemistry.ResultsCompared to patients with no exposure, patients with exposure showed higher counts of α4 and α7 nicotinic acetylcholine receptors (t-test, p < 0.05). However, in patients with no exposure, multivariate analysis showed gender dimorphism, with lower counts in males than in females, and no influence from other variables (analysis of covariance, p > 0.05).ConclusionExposure to cigarette tobacco smoke may induce increased counts of α4 and α7 nicotinic acetylcholine receptors in nasal polyps of adults, with lower counts in males than females without exposure to tobacco smoke.

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