The blotted membranes were visualized using enhanced chemiluminescence reagents (GE Healthcare). increased migration and invasion of MDA-MB-231 cells. miR-141/200c overexpression was more effective in decreasing cell growth and promoting migration and invasion of MDA-MB-231 cells than was miR-200b/200a/429 overexpression. In addition, the overexpression of the miR-200b/200a/429 or miR-141/200c cluster led to an increase in the phosphorylation of focal adhesion kinase (FAK) and protein kinase B (AKT). Chemical inhibitors of FAK and phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/AKT suppressed the migration and invasion of MDA-MB-231 cells that was enhanced by the overexpression of the miR-200b/200a/429 or Sigma-1 receptor antagonist 2 miR-141/200c cluster. Compared to the miR-200b/200a/429 cluster-transduced MDA-MB-231 cells, the miR-141/200c cluster-transduced MDA-MB-231 cells exhibited a significant increase in vascular endothelial growth factor (VEGF)-A secretion and integrin-alphaV (integrin-V) expression. Treatment with an anti-VEGF-A-neutralizing antibody inhibited the increase in migration and invasion in both the miR-200b/200a/429- and miR-141/200c-transduced MDA-MB-231 cells but significantly reduced the phosphorylation of FAK and AKT in only the miR-141/200c cluster-transduced MDA-MB-231 cells. Conclusions Taken together, our data demonstrate a mechanism in which the miR-141/200c cluster, through FAK- and PI3K/AKT-mediated signaling by means Sigma-1 receptor antagonist 2 of increased VEGF-A secretion, promotes the migratory and invasive abilities of MDA-MB-231 cells. Electronic supplementary material The online version of this article (doi:10.1186/s12885-016-2620-7) contains supplementary material, which is available to authorized users. Keywords: Triple-negative breast cancer (TNBC), microrna-200 (miR-200), Vascular endothelial growth factor (VEGF), Migration, Invasion, Phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K), Protein kinase B (AKT), Focal adhesion kinase (FAK) Background Aberrant expression of microRNAs (miRs), which are small non-coding RNA molecules consisting of approximately 22 nucleotides, has been identified in human cancer, where the miRNA signature is usually associated with specific clinical Sigma-1 receptor antagonist 2 and biological features [1]. The microRNAs related to cancers may act as tumor suppressors or oncogenes, depending on the cancer type [2, 3]. The miR-200 family member genes are clustered at two locations in the genome: the miR-200b/200a/429 cluster and the miR-141/200c cluster [4]. The miR-200 family members repress the epithelial-to-mesenchymal transition (EMT), cancer cell migration, tumor growth, and metastasis by directly targeting specific genes, such as ZEB1, Suz12, moesin, and AP-2 [4, 5]. In contrast, the miR-200 family members have been shown to enhance the migration ability of breast cancer cells and to promote the metastatic colonization of breast cancer cells through up-regulating the expression of E-cadherin and down-regulating that of ZEB2 and Sec23a [6, 7]. In a recent study, high expression of the miR-200 family was associated with a high probability of relapse, poor survival, and distant metastasis in breast cancer patients [8]. The loss of miR-200c expression has also been related to the induction of an aggressive, invasive, and chemoresistant phenotype of nonCsmall cell lung cancer [9]. Conflicting results have been obtained in studies of the role of each miR-200 family member in repressing or enhancing cancer cell migration and invasion as well as the tumor growth and metastasis of diverse cancers, including breast cancer [10, 11]. Triple-negative breast cancer (TNBC) lacking estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) expression, is a highly invasive and metastatic form of breast cancer with a generally poorer prognosis than that of other breast cancer subtypes [12]. It’s important to Sigma-1 receptor antagonist 2 develop fresh treatment strategies predicated on a better knowledge of the root systems regulating the intense behavior of TNBCs. TNBCs communicate the miR-200 family at a lesser level than perform additional subtypes PROCR of breasts tumor considerably, such as for example HER2-positive or ER-positive breast tumor [13]. Only a small amount of the miR-200 focus on genes that get excited about breasts tumor cell migration.