Article Abstract

SU6668 inhibits the proliferation and motility of colorectal cancer cells by inducing cycle arrest, and promotes their apoptosis

Authors: Jianyong Yu, Li Li, Chengsuo Huang

Abstract

Background: The multi-targeted angiogenesis inhibitor SU6668 has demonstrated promising therapeutic effects on the progression of hematologic malignancies and certain solid tumors. Previous studies reported that SU6668 inhibited the liver metastasis of both human and mouse colon cancer xenografts via its antiangiogenic effect. This study was conducted to determine the effect of SU6668 on the proliferation, migration, and invasion of colorectal cancer cells and their rates of apoptosis.
Methods: SW480 and SW620 cells were treated with various concentrations of SU6668 (15, 30, and 45 μM, respectively), and their proliferation was examined by CCK-8 and EdU assays. Changes in the clone formation ability of colorectal cancer cells treated with SU6668 were assessed with colony formation assays. The effects of SU6668 on cell cycle progression and apoptosis were detected by flow cytometry. Hoechst staining was used to determine the rates of apoptotic cell death. Western blot was used to analyze the relative levels of Bax, caspase-3 and Bcl-2 protein expression. Matrigel invasion assays were used to assess the effects of SU6668 on colorectal cancer cell migration and invasion capabilities.
Results: SU6668 inhibited the proliferation and clone formation ability of colorectal cancer cells in a dose- and time-dependent manner. SU6668 also induced G0/G1 cell cycle arrest and cell apoptosis. The expression levels of apoptosis-related proteins (Bax and caspase-3) were enhanced, while the level of Bcl-2 expression was significantly decreased in SU6668-treated colorectal cancer cells. SU6668 significantly inhibited the migration and invasion of colorectal cancer cells.
Conclusions: SU6668 can inhibit the proliferation, migration, and invasion of colorectal cancer cells, as well as their ability for colony formation. SU6668 inhibited cell proliferation by inducing G1 cell cycle arrest and induced apoptosis by activating Bax and caspase-3.

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