The effects of cigarette smoking extracts on cell cycle and tumor spread: novel evidence

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.

Abstract

There is evidence of cancerogenic effects of cigarette smoke compounds. Cigarette smoke extract is a tobacco condensate obtained by filtration processes. Studies have shown that it can modify the cell cycle, inducing uncontrolled cell proliferation. This effect occurs through activation of genetic and epigenetic pathways and increasing the expression of proteins involved in inflammation. The pathways activated by cigarette smoke extract open up opportunities for researchers to develop new targeted therapies toward the specific molecules involved. Furthermore, the effects exerted by cigarette smoke extract on normal epithelial cells hold potential for use in the development of prevention medicine and early cancer diagnosis.