Zhouquan Wang1, Hehe Liao, Zhiping Deng, Po Yang, Ning Du, Yunfeng Zhanng, Hong Ren. 1. Department of Chest Surgery, The First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an 710061, China; Department of Tumor, SenGong Hospital of Shaanxi, Xi'an 710300, China.
Abstract
BACKGROUND: An increasing number of studies have shown that miRNAs are commonly deregulated in human malignancies, but little is known about the function of miRNA-205 (miR-205) in human breast cancer. The present study investigated the influence of miR-205 on breast cancer malignancy. METHODS: The expression level of miR-205 in the MCF7 breast cancer cell line was determined by quantitative (q)RT-PCR. We then analyzed the expression of miR-205 in breast cancer and paired non-tumor tissues. Finally, the roles of miR-205 in regulating tumor proliferation, apoptosis, migration, and target gene expression were studied by MTT assay, flow cytometry, qRT-PCR, Western blotting and luciferase assay. RESULTS: miR-205 was downregulated in breast cancer cells or tissues compared with normal breast cell lines or non-tumor tissues. Overexpression of miR-205 reduced the growth and colony-formation capacity of MCF7 cells by inducing apoptosis. Overexpression of miR-205 inhibited MCF7 cell migration and invasiveness. By bioinformation analysis, miR-205 was predicted to bind to the 3' untranslated regions of human epidermal growth factor receptor (HER)3 mRNA, and upregulation of miR-205 reduced HER3 protein expression. CONCLUSION: miR-205 is a tumor suppressor in human breast cancer by post-transcriptional inhibition of HER3 expression.
BACKGROUND: An increasing number of studies have shown that miRNAs are commonly deregulated in humanmalignancies, but little is known about the function of miRNA-205 (miR-205) in humanbreast cancer. The present study investigated the influence of miR-205 on breast cancer malignancy. METHODS: The expression level of miR-205 in the MCF7 breast cancer cell line was determined by quantitative (q)RT-PCR. We then analyzed the expression of miR-205 in breast cancer and paired non-tumor tissues. Finally, the roles of miR-205 in regulating tumor proliferation, apoptosis, migration, and target gene expression were studied by MTT assay, flow cytometry, qRT-PCR, Western blotting and luciferase assay. RESULTS:miR-205 was downregulated in breast cancer cells or tissues compared with normal breast cell lines or non-tumor tissues. Overexpression of miR-205 reduced the growth and colony-formation capacity of MCF7 cells by inducing apoptosis. Overexpression of miR-205 inhibited MCF7 cell migration and invasiveness. By bioinformation analysis, miR-205 was predicted to bind to the 3' untranslated regions of humanepidermal growth factor receptor (HER)3 mRNA, and upregulation of miR-205 reduced HER3 protein expression. CONCLUSION:miR-205 is a tumor suppressor in humanbreast cancer by post-transcriptional inhibition of HER3 expression.