Abstract
Cigarette smoking is a major preventable risk factor for lung cancer, contributing to lung cancer progression and metastasis. Moreover, cigarette smoking correlates with increased metastasis frequency of pancreatic, breast and bladder cancer. The aim of this review was to examine the role of cigarette smoke extract in cell cycle and cancer progression. Clinical impact and the effects of cigarette smoke extract on carcinogenesis are discussed. 98 of the over 5000 chemicals in tobacco smoke are known carcinogens that can act on cancer genes such as K-RAS and p53. Through various mechanisms these compounds can activate molecules involved in the cell cycle, such as cyclins, and molecules involved in apoptosis and autophagy, such as Beclin-1 or LC3B. A search of the literature, including in vitro and in vivo studies, was carried out and the results summarized.
Highlights
Tumorigenic functionResearch seeking to understand the effects of smoking on cells in vitro, including apoptosis, inflammation, metastasis and proliferation [5]
Smoking-induced carcinogenesis is a result of genetic mutation or the activation of protein receptors that in turn activate kinases responsible of cell growth and uncontrolled proliferation
A Cigarette smoke extracts (CSEs) compound, induces phosphorylation of GSK kinase favoring the action of proteins (β-catenin) that dysregulate the cell cycle
Summary
Research seeking to understand the effects of smoking on cells in vitro, including apoptosis, inflammation, metastasis and proliferation [5]. MTA1 activity can be considered as a smoking-induced marker of invasiveness [12] Another factor tightly linked with tumor progression is the RNA-binding motif protein 5 (RBM5), whose gene is named LUCA-15 or H37, which is a direct modulator of cell cycle. It was demonstrated that in vitro exposure to CSE reduced RBM5 mRNA and protein levels both in human bronchial epithelial cells (BEAS-2B) and in cancerous cells (A549) [15]. Long intergenic noncoding RNA (linc00152) serum level in CSE-exposed individuals was increased in a dose-dependent manner It is involved in regulation of cell adhesion, epithelial transition and other malignant phenotypes, which in turn, affected metastasis in vivo. In order to confirm GOLPH3 involvement after smoke exposure, western blot was performed in vivo on samples from NSCLC-diagnosed patients This demonstrated high levels of GOLPH3 and mouse lungs exposed to NNK showed high titre in GOLPH3 mRNA and proteins. In the study presented by Liao et al TGF-β1, MMP3, Smad and invasive cells were reduced after exposure to a blocker of TGF-β1, showing that TGF-β1 and MMP3 are main actors in lung cancer invasiveness and share a potentially procarcinogenetic pathway [63]
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