miR‑155 promotes proliferation and epithelial‑mesenchymal transition of MCF‑7 cells
- Xiaoyan Liu
- Yongjun Li
- Zhuo Li
- Tian Hou
Affiliations: Department of Breast Surgery, Affiliated Hospital of Hebei University of Engineering, Handan, Hebei 056200, P.R. China, Department of Imaging, Affiliated Hospital of Hebei University of Engineering, Handan, Hebei 056200, P.R. China, Department of Orthopedics, Hebei Chest Hospital, Shijiazhuang, Hebei 050041, P.R. China, Department of Surgery, Xinganmeng People's Hospital, Ulanhot, Inner Mongolia 137400, P.R. China
- Published online on: January 15, 2021 https://doi.org/10.3892/etm.2021.9650
Copyright: © Liu
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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.