4.4 Article

Aberrant expression of miR-9 in benign and malignant breast tumors

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MOLECULAR AND CELLULAR PROBES
卷 30, 期 5, 页码 279-284

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ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.mcp.2016.10.005

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Benign; Breast cancer; Malignant; miR-9; Signaling pathway

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Purpose: MicroRNAs (miRNAs) are involved in the progression of breast cancer (BC). miR-9 has been reported to be correlated with either favorable or unfavorable events in BC. This study was aimed to evaluate the expression level of miR-9 in human breast tissues, including benign and malignant tumor samples and also healthy tissue. Materials and methods: The expression level of miR-9 was analyzed in 10 normal breast tissues, 30 malignant, and 30 benign breast tumor tissue samples using RT-PCR and qPCR. In addition, bioinformatics assessment upon miR-9 functionality in BC cells was performed. Results and discussion: The miR-9 expression level was downregulated in tumor tissues, including benign and malignant compared to the healthy tissue was observed (P value, < 0.0001; fold change, -1.37). In addition, miR-9 expression level was reduced in benign tumors compared with malignant tumors (P value, < 0.0001; fold change, -1.35). Moreover, according to the AUCs (area under curve) of receiver operating characteristic (ROC) curves, miR-9 showed significant capability for distinguishing benign from healthy, malignant from healthy, benign from malignant, and tumor from health tissues. Furthermore, pathways in cancer, p53 signaling pathway, and focal adhesion were manifested by computational analysis as miR-9 related signaling pathways which have logical association with experimental observations. Conclusion: In conclusion, downregulation of miR-9 in benign tumors vs healthy tissue and its over expression in malignant tumors vs benign tumors suggest paradoxical functionality for this miRNA. Our results shed additional information on controversial expression pattern of miR-9 depending on different progression level of BC. (C) 2016 Elsevier Ltd. All rights reserved.

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