Epigenetic and molecular mechanisms of tumorigenesis caused by tobacco smoke

Horvat, Luka (2012) Epigenetic and molecular mechanisms of tumorigenesis caused by tobacco smoke. Bachelor's thesis, Faculty of Science > Department of Biology.

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Abstract

This paper described the basic processes responsible for the emergence and development of tumors (tumorigenesis) and their mechanisms. All the described processes were associated with tobacco smoke as the carcinogen. There are many (over 62) components of tobacco smoke with carcinogenic potential; however, most research has focused on three components: nicotine, 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and polycyclic aromatic hydrocarbons (PAH). Nicotine and NNK are specific to tobacco smoke while the PAH compounds are found in the environment as a result of industrial pollution. In this paper genotoxic mechanisms were described, but the focus was placed on the the very important non-genotoxic i.e. epigenetic mechanisms of tumorigenesis. The most common epigenetic changes are related to the changes in DNA methylation, histone modifications, and noncoding RNA molecule, which serve to regulate important cellular functions. These modifications lead to changes in the expression of proteins essential for normal cell cycle. Mechanisms that cause tumor promotion and progression are complex and involve many molecular targets, such as receptors, cell cycle regulators, mitogen-activated protein kinases, apoptosis mediators, angiogenic factors, and invasion and metastasis mediators. Among the receptors, nAChR, β-AR, and AhR have the closest association with cigarette smoke-induced carcinogenesis. Over expression or activation of these receptors may result in a release of neurotransmitters and growth factors that participate in apoptosis inhibition, cell proliferation, angiogenesis, cancer cell invasion and metastasis. Signaling pathways PI3K/AKT, Stat3, and ERK1/2 play an important role in the carcinogenetic processes. They are also common paths affected by cigarette smoke components, including nicotine, NNK, and PAHs. In addition, PKC, AKT, ERK, and COX-2 signaling pathways are involved in both promotion and progression stages of tumorigenesis caused by cigarette smoke. It is assumed that these molecules could be used as potential targets for future development of therapies and medicines against tumors.

Item Type: Thesis (Bachelor's thesis)
Supervisor: Pavlica, Mirjana
Date: 2012
Number of Pages: 17
Subjects: NATURAL SCIENCES > Biology
Divisions: Faculty of Science > Department of Biology
Depositing User: Silvana Šehić
Date Deposited: 13 Oct 2014 10:31
Last Modified: 13 Oct 2014 10:31
URI: http://digre.pmf.unizg.hr/id/eprint/3015

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