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

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          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.


          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.

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          Most cited references 54

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          Molecular chaperones in cellular protein folding.

          The folding of many newly synthesized proteins in the cell depends on a set of conserved proteins known as molecular chaperones. These prevent the formation of misfolded protein structures, both under normal conditions and when cells are exposed to stresses such as high temperature. Significant progress has been made in the understanding of the ATP-dependent mechanisms used by the Hsp70 and chaperonin families of molecular chaperones, which can cooperate to assist in folding new polypeptide chains.
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            Multiple functions of p21 in cell cycle, apoptosis and transcriptional regulation after DNA damage.

            An appropriate control over cell cycle progression depends on many factors. Cyclin-dependent kinase (CDK) inhibitor p21 (also known as p21(WAF1/Cip1)) is one of these factors that promote cell cycle arrest in response to a variety of stimuli. The inhibitory effect of P21 on cell cycle progression correlates with its nuclear localization. P21 can be induced by both p53-dependent and p53-independent mechanisms. Some other important functions attributed to p21 include transcriptional regulation, modulation or inhibition of apoptosis. These functions are largely dependent on direct p21/protein interactions and also on p21 subcellular localizations. In addition, p21 can play a role in DNA repair by interacting with proliferating cell nuclear antigen (PCNA). In this review, we will focus on the multiple functions of p21 in cell cycle regulation, apoptosis and gene transcription after DNA damage and briefly discuss the pathways and factors that have critical roles in p21 expression and activity.
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              Nrf2 is essential for protection against acute pulmonary injury in mice.

              Nrf2 is a member of the "cap 'n' collar" family of transcription factors. These transcription factors bind to the NF-E2 binding sites (GCTGAGTCA) that are essential for the regulation of erythroid-specific genes. Nrf2 is expressed in a wide range of tissues, many of which are sites of expression for phase 2 detoxification genes. Nrf2(-/-) mice are viable and have a normal phenotype under normal laboratory conditions. The NF-E2 binding site is a subset of the antioxidant response elements that have the sequence GCNNNGTCA. The antioxidant response elements are regulatory sequences found on promoters of several phase 2 detoxification genes that are inducible by xenobiotics and antioxidants. We report here that Nrf2(-/-) mice are extremely susceptible to the administration of the antioxidant butylated hydroxytoluene. With doses of butylated hydroxytoluene that are tolerated by wild-type mice, the Nrf2(-/-) mice succumb from acute respiratory distress syndrome. Gene expression studies show that the expression of several detoxification enzymes is altered in the Nrf2(-/-) mice. The Nrf2(-/-) mice may prove to be a good in vivo model for toxicological studies. As oxidative damage causes DNA breakage, these mice may also be useful for testing carcinogenic agents.

                Author and article information

                Future Sci OA
                Future Sci OA
                Future Science OA
                Future Science Ltd (London, UK )
                03 May 2019
                June 2019
                : 5
                : 5
                [1 ]Cardiovascular & Thoracic Department, AOU Sant’Andrea, Sapienza – Università di Roma, Roma, Italy
                [2 ]Oncology Department, Campus Bio-Medico Università di Roma, Roma, Italy
                [3 ]Department of Medicine Clinical Research Office & Primary Care Internal Medicine, Mayo Clinic, Rochester, MN 55905, USA
                Author notes
                [* ]Author for correspondence: Tel.: +39 340 537 0336; Fax: +39 062 254 11933; f.citarella@ 123456unicampus.it
                © 2019 Fabrizio Citarella

                This work is licensed under the Creative Commons Attribution 4.0 License

                Page count
                Pages: 10


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