Abstract

ABSTRACT Introduction Recent evidence suggests that HER2 (ErbB2; Her-2/neu) influences the malignant phenotype of many cancer cells significantly. Fatty acid synthase (FASN) is frequently overexpressed in human cancers, and plays a crucial role in the carcinogenesis of various cancers. But the role of HER2 and FASN in regulating the malignant phenotype of colorectal cancer cells is still indefinite. Methods Caco-2 cells with a high expression of both HER2 and FASN and a high transfection efficiency were selected for functional characterization. Caco-2 cells were stably transfected with the HER2 specific RNAi plasmid, the FASN specific RNAi plasmid and the negative control RNAi plasmid, respectively, and followed by the RT-qPCR and Western Blot to examine the expression of HER2 and FASN. The MTT and Colony formation assays were used to assess proliferation potential. The migration was investigated by the Transwell assay, and the apoptosis and cell cycle were assayed by the Flow cytometry. Results Notably, the expression of FASN/HER2were correspondingly downregulated upon a silence of HER2/FASN. The proliferation was decreased after a downregulation of HER2/FASN, which was consistent with an increased apoptosis rate. The migration was also impaired in HER2/FASN-silenced cells. Conclusion A downregulation of HER2/FASN effectively regulates the malignant phenotype of Caco-2 cells. It indicates that the interaction of HER2 and FASN plays a crucial role in the carcinogenesis of colorectal cancer.

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