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Background  Breast cancer has been the first death cause of cancer in women all over the world. Metastasis is believed to be the most important process for treating breast cancer. There is evidence that lncRNA  MEG3  functions as a tumor suppressor in breast cancer metastasis. However, upstream regulation of  MEG3  in breast cancer remain elusive. Therefore, it is critical to elucidate the underlying mechanism upstream MEG3 to regulate breast cancer metastasis.    Methods  We employed RT-qPCR and Western blot to examine expression level of  miR - 506 , DNMT1, SP1, SP3 and  MEG3 . Besides, methylation-specific PCR was used to determine the methylation level of  MEG3  promoter. Wound healing assay and transwell invasion assay were utilized to measure migration and invasion ability of breast cancer cells, respectively.    Results  SP was upregulated while  miR - 506  and  MEG3  were downregulated in breast tumor tissue compared to adjacent normal breast tissues. In addition, we found that  miR - 506  regulated DNMT1 expression in an SP1/SP3-dependent manner, which reduced methylation level of  MEG3  promoter and upregulated  MEG3  expression. SP3 knockdown or  miR - 506  mimic suppressed migration and invasion of MCF-7 and MDA-MB-231 cells whereas overexpression of SP3 compromised miR-506-inhibited migration and invasion.    Conclusions  Our data reveal a novel axis of  miR - 506 /SP3/SP1/DNMT1/ MEG3  in regulating migration and invasion of breast cancer cell lines, which provide rationales for developing effective therapies to treating metastatic breast cancers.

miR-506 attenuates methylation of lncRNA MEG3 to inhibit migration and invasion of breast cancer cell lines via targeting SP1 and SP3