Yinjue Yu1, Linfeng Zhao1, Rong Li1. 1. Department of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Abstract
OBJECTIVE: To investigate the effect of medium-chain acyl-CoA dehydrogenase (ACADM) on invasion and metastasis of breast cancer cells and explore the underlying mechanism. METHODS: A large cancer genome database was used to analyze the expression of ACADM in breast cancer tissues and normal tissues. The proliferation, migration and invasion of cultured breast cancer MCF-7 and T47D cells with ACADM overexpression or ACADM silencing were evaluated using MTT proliferation assay, EdU assay, Transwell chamber assay, and Boyden invasion assay; Western blotting was used to detect the protein expressions of the related pathway in the cells. In nude mouse models of tail vein metastasis of MCF-7 cells with or without ACADM overexpression, the tumor growth and tumor histopathology were observed using HE staining. RESULTS: Analysis of the Oncomine sample set showed a significantly higher expression level of ACADM in breast cancer tissues than in normal breast tissues (P < 0.05). Overexpression of ACADM obviously enhanced the migration and invasion abilities and promoted the epithelial-mesenchymal transition (EMT) of cultured MCF-7 and T47D cells; conversely, silencing of ACADM significantly suppressed the migration and invasion of the breast cancer cells. In the nude mouse models, ACADM overexpression in MCF-7 cells significantly enhanced their in vivo migration and invasion abilities. CONCLUSIONS: ACADM can promote the EMT process of breast cancer cells and improve the migration and invasion ability. ACADM is an oncogene in breast cancer.
OBJECTIVE: To investigate the effect of medium-chain acyl-CoA dehydrogenase (ACADM) on invasion and metastasis of breast cancer cells and explore the underlying mechanism. METHODS: A large cancer genome database was used to analyze the expression of ACADM in breast cancer tissues and normal tissues. The proliferation, migration and invasion of cultured breast cancer MCF-7 and T47D cells with ACADM overexpression or ACADM silencing were evaluated using MTT proliferation assay, EdU assay, Transwell chamber assay, and Boyden invasion assay; Western blotting was used to detect the protein expressions of the related pathway in the cells. In nude mouse models of tail vein metastasis of MCF-7 cells with or without ACADM overexpression, the tumor growth and tumor histopathology were observed using HE staining. RESULTS: Analysis of the Oncomine sample set showed a significantly higher expression level of ACADM in breast cancer tissues than in normal breast tissues (P &lt; 0.05). Overexpression of ACADM obviously enhanced the migration and invasion abilities and promoted the epithelial-mesenchymal transition (EMT) of cultured MCF-7 and T47D cells; conversely, silencing of ACADM significantly suppressed the migration and invasion of the breast cancer cells. In the nude mouse models, ACADM overexpression in MCF-7 cells significantly enhanced their in vivo migration and invasion abilities. CONCLUSIONS:ACADM can promote the EMT process of breast cancer cells and improve the migration and invasion ability. ACADM is an oncogene in breast cancer.
Entities:
Keywords:
breast cancer; invasion; medium chain acyl-CoA dehydrogenase; migration
Authors: Regina Ensenauer; Jennifer L Winters; Patricia A Parton; David F Kronn; Jong-Won Kim; Dietrich Matern; Piero Rinaldo; Si Houn Hahn Journal: Genet Med Date: 2005 May-Jun Impact factor: 8.822