The relative concentrations of breast cancer-associated miR10b, miR34a, miR141 and miR155 were measured in the blood serum of 89 patients with primary breast cancer (M0, n = 59) and metastatic disease (M1, n = 30), and 29 healthy women by a TaqMan MicroRNA Assay.
The serum miR-141 level was found to be positively correlated with alkaline phosphatase (ALP) level in patients with skeletal metastasis, using Pearson's bivariate correlation test.
Taken together, our results suggest that PELP1 regulates tumor metastasis by controlling the expression and functions of the tumor metastasis suppressors miR-200a and miR-141.
Here, we demonstrate by ectopic expression and gene silencing that the proto-oncogene c-Myb activates the expression of the 5 members of miR200 family (miR200b, miR200a, miR429, miR200c and miR141) that are involved in the control of epithelial-mesenchymal transition (EMT) and metastasis in many types of cancers.
miR-141 serves as a potential biomarker for discriminating ccRCC from normal tissues and a crucial suppressor of ccRCC cell proliferation and metastasis by modulating the EphA2/p-FAK/p-AKT/MMPs signaling cascade.
In conclusion, miR-141 can be considered an important cancer suppressor gene of renal cancer by inhibiting proliferation and metastasis of renal cancer cells.
In addition, decreased miR-141-3p levels were detected in the multiple tumor nodes group ( P = .004), the metastasis group ( P < .001), and the advanced TNM stage group ( P = .01), compared to the single tumor nodes group, the nonmetastasis group, and the early TNM stage group.
MiR-200b, miR-200c, and miR-141 have been confirmed to be related to tumor metastasis. miR-141 levels in serum from experimental group was higher significant compared to control group (p = 0.024). miR-200b levels in serum from experimental group was significantly increased compared to control group (p = 0.031).
Levels of miR-200c and miR-141 were lower in Foxp3 <sup>sf/+</sup> tumor cells than in normal breast epithelial cells, but plasma levels of miR-200c and miR-141 in the Foxp3 <sup>sf/+</sup> mice increased during tumor progression and metastasis.
Clinically, prostate cancer (PCa) exhibits a high avidity to metastasize to bone. miR-141-3p is an extensively studied miRNA in cancers and downregulation of miR-141-3p has been widely reported to be involved in the progression and metastasis of several human cancer types.
In this study, we performed a series of experiments <i>in vivo</i> and <i>in vitro</i> to determine whether exosomal miR-141-3p from MDA PCa 2b cells regulates osteoblast activity to promote osteoblastic metastasis.
Our data show that forced expression of miR-141 or miR-200c suppressed invasion and metastasis of PDAC cells both in vitro and in xenograft and identified WIPF1 as a direct target of miR-141 and miR-200c.
Taken together, these data not only demonstrate an anti-angiogenic effect of miR-141, further strengthening the critical role of miR-200 family in the process of angiogenesis, but also provides a valuable cancer therapeutic target to control both angiogenesis and EMT, two essential steps in tumor growth and metastasis.
Patients with distant metastasis had significantly higher expression levels of microRNA-183 and microRNA-141 than patients without distant metastasis (p<0.01).