Affiliations: [a] Department of Medical Ultrasonics, The Second Hospital of Lanzhou University, Lanzhou, Gansu, China | [b] Department of Oncology, The Third people’s Hospital of Jinan, Jinan, Shandong, China | [c] Department of Oncology, The Second Hospital of Lanzhou University, Lanzhou, Gansu, China
Correspondence:
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Corresponding author: Pei-Wu Li, Department of Oncology, The Second Hospital of Lanzhou University, Gansu, China. Tel./Fax: +86 0931 8942874; E-mail: jqwanggs@163.com.
Abstract: Background:Rac1, the better characterized Rac subfamily member, can regulate a large variety of different functions, including the organization of the actin cytoskeleton, cell migration, cell cycle progression, and cell survival through engagement of specific effectors. However, very little is currently known about the expression of Rac1 in colorectal cancer cells and the roles of Rac1 in the cell cycle progression and cell survival of human colorectal cancer cells. Objective:To assess the change of cytoskeleton and cell cycle in Lovo (human colorectal cancer) cell via deletion of Rac1 with RNA interference. Methods:Rac1 protein of all selected human colorectal cancer cells and in human colorectal tissue was detected by Western blotting, Rac1-shRNA was used to silence the Rac1 to reduce its expression specifically in Lovo cells. Results:Rac1 protein was overexpressed in human colorectal cancer cells and in human colorectal tissue, RNA interference-mediated deletion of Rac1 strongly prolonged cell cycle progression and enhanced cell apoptosis of Lovo cells in vitro. Conclusions:depletion of Rac1 by the use of RNAi can arrest Lovo Cells in G0/G1 and induce LoVo cells apoptosis.
