在人體中存在著許多種機械力而拉伸力即屬於其中一種,循環拉伸存在於如:心臟、肺臟等等…在過去已知循環拉伸會對細胞的增殖、分化及基因調控造成影響且在維持組織恆定上扮演重要的角色。本實驗分別對人類肺部纖維母細胞NHLF和肺腺癌細胞A549給予機械循環拉伸處理,並探討纖維化程度、癌細胞於三維環境中的侵襲以及和周遭免疫細胞的互動。結果顯示給予一定程度的循環拉伸會使肺部纖維母細胞表現較多的成肌纖維母細胞標誌物α-SMA。在癌細胞部份,循環拉伸對於三維肺腺癌細胞球在膠原蛋白水凝膠中的侵襲有抑制的現象,而使用經由形變量10%、頻率0.21 hz拉伸的A549條件培養基處理的M0未成熟巨噬細胞在24、48小時有較明顯的M1標誌物TLR2、IL-1β、TNF-α上升及M2標誌物CD206下降,這說明經拉伸的A549可能具有促使巨噬細胞朝M1表型發展之能力。;There are many mechanical forces in the human body, and stretching is one of them. Cyclic stretching exists in the heart, lungs, etc. In the past, it was known that cyclic stretching would affect cell proliferation, differentiation, and gene regulation. And it plays an important role in tissue maintenance. In this study, human lung fibroblasts NHLF and lung adenocarcinoma cells A549 were treated with mechanical circulation stretching, and the degree of fibrosis, the invasion of cancer cells in a three-dimensional environment and the interaction with surrounding immune cells were explored. The results show that given a certain degree of cyclic stretching can make lung fibroblasts express more myofibroblast marker α-SMA. In the cancer cell part, cyclic stretching can inhibit the invasion of lung adenocarcinoma spheroid in the collagen hydrogel. After stretched A549 conditioned medium with a magnitude of 10% and a frequency of 0.21 hz treating, Na?ve macrophages have obvious M1 markers TLR2, IL-1β, TNF-α increase and M2 marker CD206 decrease at 24 and 48 hours, which indicates that the stretched A549 may promote the macrophages to move toward M1 phenotype.