Xiaowen Wang1, Xin Zhou2, Fanye Zeng3, Xiaotang Wu4, Hua Li5. 1. Department of the Second Ward of Breast Surgery, The Third Clinical Medical College of Xinjiang Medical University, Xinjiang, China. 2. Department of the Second Ward of Pulmonary Medicine, The Third Clinical Medical College of Xinjiang Medical University, Xinjiang, China. 3. Department of Second Oncology, The Fourth Clinical Medical College of Xinjiang Medical University, Xinjiang, China. 4. Shanghai Engineering Research Center of Pharmaceutical Translation, Shanghai, China. 5. Department of Surgical Oncology, Tangshan Gongren Hospital, Hebei Medical University, 27 Wenhua Road, Tangshan, 063000, China. L1huaaaaaaaaa@163.com.
Abstract
OBJECTIVE: To investigate the mechanism of miR-485-5p inhibiting breast cancer cells by targeting MUC1. METHODS: Differentially expressed genes (DEGs) in breast cancer tissues were analyzed using breast cancer tissue microarrays (TMA) in the GEO database. Differential expression of MUC1 in breast cancer tissue samples was detected by TCGA database. qRT-PCR was used to detect the expression of MUC1 and miR-485-5p in human normal breast epithelial cell lines and human breast cancer cell lines. Bioinformatics was applied to analyze targeted binding site of miR-485-5p and MUC1 and their targeted relationship was identified by dual luciferase assay. The proliferation ability of breast cancer cells was detected by CCK-8 assay. Cell apoptosis was detected by flow cytometry. The ability of cell migration was measured by scratch healing test. Transwell assay was used to detect the invasion ability of cells. The protein expression levels of MUC1 and EMT-related molecules (E-cadherin, N-cadherin and Vimentin) were detected by Western blot. RESULTS: MUC1 was highly expressed in breast cancer tissue samples and breast cancer cell lines, while miR-485-5p was lowly expressed. Overexpression of miR-485-5p inhibits cell viability and invasion and migration of breast cancer cell line MCF-7 and promotes apoptosis. The same results were obtained by silencing the expression of MUC1. MiR-485-5p targets to bind to the 3'-UTR region of MUC1 and negatively regulates the expression of MUC1. Overexpressing MUC1 while overexpressing miR-485-5p reversed the inhibitory effect of miR-485-5p on breast cancer and inhibited EMT. CONCLUSION: MiR-485-5p can down-regulate the expression of MUC1, thus inhibit the proliferation, invasion and migration of breast cancer cells and promote cell apoptosis.
OBJECTIVE: To investigate the mechanism of miR-485-5p inhibiting breast cancer cells by targeting MUC1. METHODS: Differentially expressed genes (DEGs) in breast cancer tissues were analyzed using breast cancer tissue microarrays (TMA) in the GEO database. Differential expression of MUC1 in breast cancer tissue samples was detected by TCGA database. qRT-PCR was used to detect the expression of MUC1 and miR-485-5p in human normal breast epithelial cell lines and humanbreast cancer cell lines. Bioinformatics was applied to analyze targeted binding site of miR-485-5p and MUC1 and their targeted relationship was identified by dual luciferase assay. The proliferation ability of breast cancer cells was detected by CCK-8 assay. Cell apoptosis was detected by flow cytometry. The ability of cell migration was measured by scratch healing test. Transwell assay was used to detect the invasion ability of cells. The protein expression levels of MUC1 and EMT-related molecules (E-cadherin, N-cadherin and Vimentin) were detected by Western blot. RESULTS:MUC1 was highly expressed in breast cancer tissue samples and breast cancer cell lines, while miR-485-5p was lowly expressed. Overexpression of miR-485-5p inhibits cell viability and invasion and migration of breast cancer cell line MCF-7 and promotes apoptosis. The same results were obtained by silencing the expression of MUC1. MiR-485-5p targets to bind to the 3'-UTR region of MUC1 and negatively regulates the expression of MUC1. Overexpressing MUC1 while overexpressing miR-485-5p reversed the inhibitory effect of miR-485-5p on breast cancer and inhibited EMT. CONCLUSION:MiR-485-5p can down-regulate the expression of MUC1, thus inhibit the proliferation, invasion and migration of breast cancer cells and promote cell apoptosis.
Entities:
Keywords:
Breast cancer; EMT; Invasion and migration; MUC1; MiR-485-5p; Proliferation