Elucidation of oral cancer cell proliferation mechanism by nicotine and enlightenment of smoking cessation based on scientific evidence.

2018 Fiscal Year Final Research Report

• Project/Area Number: 15K20853
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Pathobiological dentistry/Dental radiology; Surgical dentistry
• Research Institution: Tohoku University
• Principal Investigator: Nishioka Takashi 東北大学, 歯学研究科, 助教 (50641875)
• Project Period (FY): 2015-04-01 – 2019-03-31
• Keywords: ニコチン / 口腔がん

Outline of Final Research Achievements

In this study, I focused on the nicotine, which is one of the main components of tobacco. Although, the nicotine is present in high concentrations in the bloodstream of smokers, its effect on carcinogenesis is not clear yet. The nicotine was used to examine the effect the cell growth, division and differentiation of the oral cancer cells. The oral cancer cells were stimulated by nicotine, cells were analyzed using molecular biological techniques such as Western blotting. The results showed that the nicotine induced the phosphorylation of epidermal growth factor receptor (EGFR) through the nicotinic acetylcholine receptor (nAChR), and its downstream molecular promoter activation proteins were activated. These results suggest that the nicotine was activated the cell proliferation signals and might be potential to promote the proliferation and division in oral cancer cells.

Free Research Field

口腔診断・口腔内科・歯科放射線

Academic Significance and Societal Importance of the Research Achievements

種々の病気に対し、タバコは明らかなリスクファクターとして認識され、単一で最大の生活習慣病の原因である。特に、口腔がんは発生部位である口腔の特殊性から、摂食・咀嚼・嚥下障害、発音障害、味覚障害など重要な口腔機能が障害されることにより患者のQOLは著しく低下する。本研究はタバコの構成主成分の1つであるニコチンをターゲットに実験を遂行し、ニコチンが口腔がん細胞の増殖促進に有意に関連することが示された。さらなるエビデンスの集積は必要であるが、本成果は基礎的な分子メカニズムの解明に基づく禁煙の啓蒙につながり、健康長寿の観点からも社会に貢献しうると考える。