Yubao Xue1, Wenjing Xu2, Wei Zhao3, Wei Wang4, Dahong Zhang5, Ping Wu6. 1. Department of Oncology, Huai'an Hospital, Xuzhou Medical University, Huai'an 223002, China. 2. Department of laboratory, Huaiyin Hospital of huai'an city, Huai'an 223300, China. 3. Department of laboratory, Nanjing Maternity and Child Health Care Hospital, Nanjing 210000, China. 4. Department of Pathology, Nanjing Maternity and Child Health Care Hospital, Nanjing 210000, China. 5. Department of Oncology, Hua'an First People's Hospital, Nanjing Medical Unversity, Huai'an 223300, China. Electronic address: zhangdahonghong@163.com. 6. Department of Pathology, Huai'an Maternity and Child Health Care Hospital, Huai'an 223002, China. Electronic address: wuping909@163.com.
Abstract
BACKGROUND: MicroRNAs act as posttranscriptional regulators of gene expression in many biological processes, which played a vital role in regulation cancer cells epithelial-to-mesenchymal transition and metastasis. The deregulation of miR-381 has been identified in breast cancer. However, the role and mechanism of miR-381 in breast cancer have not been completely unexplored. METHODS: Total RNA was extracted from the tissues of 27 patients with breast cancer and two breast cancer cell lines, respectively. The expression levels of miR-381 were examined by quantitative real-time PCR. The stable overexpress or silence miR-381 expression cells lines and control cells line were constructed by lentivirus infection. Subsequently, cell proliferation, cell migration, invasion assay and western blot assay were performed to detect the biological functions of miR-381 in vitro. Moreover, a luciferase reporter assay was conducted to confirm target associations. RESULTS: In this study, we validated the lower expression of miR-381 in breast cancer tissues than their adjacent non-neoplastic tissues in 27 breast cancer patients. The result also showed that miR-381 was lowly expressed in breast cancer cell lines MCF-7 and MDA-MB-231 than human epithelial cell line MCF-10A. The miR-381 expression was significantly up-regulated under exogenous miRNA-381 treatment in MCF-7 and MDA-MB-231 cells analyzed by quantitative real-time PCR. The results also indicated that an inverse correlation existed between miR-381 expression level and breast cancer cell proliferation, epithelial-to-mesenchymal transition and metastasis. Furthermore, miR-381 was predicted as a regulatory miRNA of CXCR4 in breast cancer, and the data analysis revealed that there was a negatively relationship between miR-381 and CXCR4 expression in breast cancer tissues from the patients. miR-381 played an important role in breast cancer cells proliferation, epithelial-to-mesenchymal transition and metastasis by targeting CXCR4. CONCLUSIONS: This present study revealed that miR-381 might be considered as a novel therapeutic target for breast cancer treatment.
BACKGROUND: MicroRNAs act as posttranscriptional regulators of gene expression in many biological processes, which played a vital role in regulation cancer cells epithelial-to-mesenchymal transition and metastasis. The deregulation of miR-381 has been identified in breast cancer. However, the role and mechanism of miR-381 in breast cancer have not been completely unexplored. METHODS: Total RNA was extracted from the tissues of 27 patients with breast cancer and two breast cancer cell lines, respectively. The expression levels of miR-381 were examined by quantitative real-time PCR. The stable overexpress or silence miR-381 expression cells lines and control cells line were constructed by lentivirus infection. Subsequently, cell proliferation, cell migration, invasion assay and western blot assay were performed to detect the biological functions of miR-381 in vitro. Moreover, a luciferase reporter assay was conducted to confirm target associations. RESULTS: In this study, we validated the lower expression of miR-381 in breast cancer tissues than their adjacent non-neoplastic tissues in 27 breast cancerpatients. The result also showed that miR-381 was lowly expressed in breast cancer cell lines MCF-7 and MDA-MB-231 than human epithelial cell line MCF-10A. The miR-381 expression was significantly up-regulated under exogenous miRNA-381 treatment in MCF-7 and MDA-MB-231 cells analyzed by quantitative real-time PCR. The results also indicated that an inverse correlation existed between miR-381 expression level and breast cancer cell proliferation, epithelial-to-mesenchymal transition and metastasis. Furthermore, miR-381 was predicted as a regulatory miRNA of CXCR4 in breast cancer, and the data analysis revealed that there was a negatively relationship between miR-381 and CXCR4 expression in breast cancer tissues from the patients. miR-381 played an important role in breast cancer cells proliferation, epithelial-to-mesenchymal transition and metastasis by targeting CXCR4. CONCLUSIONS: This present study revealed that miR-381 might be considered as a novel therapeutic target for breast cancer treatment.
Authors: Paula L Farré; Georgina D Scalise; Rocío B Duca; Guillermo N Dalton; Cintia Massillo; Juliana Porretti; Karen Graña; Kevin Gardner; Paola De Luca; Adriana De Siervi Journal: Oncotarget Date: 2018-02-13