Role of water-pipe smoking in breast cancer progression
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College of Medicine, Qatar University, Doha, Qatar
Biomedical Research Centre, Qatar University, Doha, Qatar
Oncology Department, McGill University, Montreal, Canada
Publication date: 2018-10-03
Corresponding author
Ala-Eddin Al Moustafa   

College of Medicine, Qatar University, Doha, Qatar
Tob. Induc. Dis. 2018;16(Suppl 3):A38
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Aim and objective:
With the increasing popularity of water-pipe smoking (WPS), it is critical to comprehend how WPS may affect women’s health. The main goal of this study is to identify the potential outcome of WPS on human breast cancer progression.

Two breast cancer cell lines, MCF7 and BT20, were used in this investigation. We explored the outcome of WPS on cell morphology and cell invasion using inverted microscope and invasion chambers. On the other hand, Western blot was employed to study the expression patterns of key control genes of cell adhesion and invasion.

Our data reveal that WPS induces epithelial-mesenchymal transition (EMT) of MCF7 and BT20 breast cancer cell lines; thus, WPS enhances cell invasion ability of both cell lines in comparison with their matched controls. More significantly, WPS provokes a down- and up-regulation of E-cadherin and focal adhesion kinase (FAK), respectively, which are important key regulators of cancer progression genes. Finally, our data point out that WPS incites the activation of Erk1/Erk2, which could be behind the stimulation of EMT and invasion as well as the deregulation of E-cadherin and FAK expression.

Our data show, for the first time, that WPS initiates EMT and stimulates cell invasion of breast cancer cells, which could incite metastatic development in breast cancer patients. Thus, we believe that further studies, both in vitro and in vivo, are required to elucidate the pathogenic outcome of WPS on cancer progression of several human carcinomas including breast, lung and oral.

Results from this report display for the first time that WPS can induce EMT and stimulate cell invasion of human breast cancer cells, consequently deregulating E-cadherin and FAK expression patterns in these cell models. Moreover, the study reveals that this effect can occur via the activation of Erk1/Erk2 pathways.

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