Breast cancer (BC) is the second leading cause of cancer-associated deaths among women worldwide. Increasing evidence has indicated that microRNAs (miRNAs) have demonstrated great potential for improving the diagnosis and therapy for BC. In the present study, miRNA-155 was detected in human BC tissues using reverse transcription-quantitative (RT-q)PCR. RT-qPCR and western blot assays were used to analyze the levels of transforming growth factor β receptor type II (TGFBR2) in human BC tissues. MCF-7 cells were cultured and treated with miR-155 inhibitor and an MTT assay was performed to determine the role of miR-155 on the proliferation of MCF-7 cells. Subsequently, TGFBR2 and epithelial-mesenchymal transition ... More
Breast cancer (BC) is the second leading cause of cancer-associated deaths among women worldwide. Increasing evidence has indicated that microRNAs (miRNAs) have demonstrated great potential for improving the diagnosis and therapy for BC. In the present study, miRNA-155 was detected in human BC tissues using reverse transcription-quantitative (RT-q)PCR. RT-qPCR and western blot assays were used to analyze the levels of transforming growth factor β receptor type II (TGFBR2) in human BC tissues. MCF-7 cells were cultured and treated with miR-155 inhibitor and an MTT assay was performed to determine the role of miR-155 on the proliferation of MCF-7 cells. Subsequently, TGFBR2 and epithelial-mesenchymal transition (EMT)-associated molecules were analyzed using RT-qPCR and western blot assays. The direct binding of miR-155 to TGFBR2 was validated using a dual luciferase assay. Higher levels of miR-155 and lower levels of TGFBR2 were expressed in human BC tissues compared with paired normal tissues. Furthermore, the expression levels of miR-155 were associated with the tumor size, TNM stage and metastasis status of BC. Transfection of MCF-7 cells with miR-155 inhibitors resulted in reduced cell proliferation and suppressed the EMT process, characterized by upregulated expression of the epithelial markers, E-cadherin and CK18, and downregulated expression of mesenchymal markers, fibronectin and smooth muscle actin α. Transfection of a miR-155 inhibitor also resulted in increased expression of TGFBR2, and miR-155 may have regulated TGFBR2 through direct binding to the 3'untranslated region of TGFBR2 as determined using a dual-luciferase assay. Based on the results of the present study, miR-155 may serve as a novel diagnostic biomarker and therapeutic target for patients with BC.
